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Immunobiology of Atherosclerosis: A Complex Net of Interactions

Beatriz Herrero-Fernandez, Raquel Gomez-Bris, Beatriz Somovilla-Crespo and 1 more

International Journal of Molecular Sciences · 2019 · Review · CC BY

doi:10.3390/ijms20215293

Abstract

Cardiovascular disease is the leading cause of mortality worldwide, and atherosclerosis the principal factor underlying cardiovascular events. Atherosclerosis is a chronic inflammatory disease characterized by endothelial dysfunction, intimal lipid deposition, smooth muscle cell proliferation, cell apoptosis and necrosis, and local and systemic inflammation, involving key contributions to from innate and adaptive immunity. The balance between proatherogenic inflammatory and atheroprotective anti-inflammatory responses is modulated by a complex network of interactions among vascular components and immune cells, including monocytes, macrophages, dendritic cells, and T, B, and foam cells; these interactions modulate the further progression and stability of the atherosclerotic lesion. In this review, we take a global perspective on existing knowledge about the pathogenesis of immune responses in the atherosclerotic microenvironment and the interplay between the major innate and adaptive immune factors in atherosclerosis. Studies such as this are the basis for the development of new therapies against atherosclerosis.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 27, 2026. Paragraph numbers are ours, so an answer can point at one.

1. Immune system

1The immune system is divided into two main branches, the innate and adaptive responses Figure 1. Innate immunity is enacted by cells of the myeloid lineage characterized by their capacity to produce a rapid and nonspecific response as a first line of defense. Innate immune cells can sense pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) through their expression of pattern recognition receptors (PRRs), such as toll-like receptors (TLRs). Innate immune cells mediate host defense responses and inflammation by producing cytokines and chemokines, activating the complement cascade and phagocytosis, or presenting antigens to activate the adaptive immune response. Prominent cells of the innate immune system include neutrophils, macrophages, and dendritic cells (DCs). The adaptive response occurs later and depends on the presentation of antigens by antigen presenting cells (APCs) and the cytokine milieu generated by the innate response. The adaptive response is specific and relies on CD4+ and CD8+ T cell activation and the production of antibodies by B cells. Natural killer T cells (NKT cells) and γδ T cells are cytotoxic T lymphocytes at the interface between innate and adaptive immunity. Abundant evidence indicates that innate and adaptive immunity both play important roles in the onset and progression of atherosclerosis. For example, Csf1−/− mice, which lack macrophage colony stimulating factor (M-CSF, also known as CSF1) are less prone to developing atherosclerosis. Moreover, mice lacking B and T cells (Rag1−/− or Rag2−/− mice lacking recombination-activating genes 1 or 2 or mice carrying the severe combined immunodeficiency (SCID) mutation) are resistant to atherosclerosis in the presence of mild hypercholesterolemia.

2. Atherosclerosis’s Epidemiology

2Atherosclerosis is the leading cause of coronary artery disease, morbidity, and mortality worldwide. Almost all individuals have atherosclerotic plaques, and even when lipids have been reduced to nominally safe levels and plaque development has been arrested, there is still a high probability of sudden thrombotic events leading to myocardial infarction or stroke. Atherosclerosis is characterized by systemic inflammation, and high levels of C-reactive protein (CRP), a circulating predictor of inflammation, are found in patients, so it has been proposed as a biomarker of atherosclerosis. Atherosclerosis is a silent disease until increased intimal thickening eventually either diminishes or blocks blood flow, inducing ischemia in downstream tissues, or triggering thrombosis after atherosclerotic plaque rupture, resulting in myocardial infarction (MI) or stroke.

3. Atherosclerosis’s Pathophysiology

3Atherosclerosis is a chronic inflammatory disease of large and medium-sized arteries, characterized by endothelial dysfunction and the accumulation of low-density lipoproteins (LDL), immune cells, and necrotic debris in the subendothelial space, resulting in the formation of an atherosclerotic plaque. LDL deposition is more likely in regions with turbulent flow and low shear stress sensed by the vascular endothelium. Turbulent flow modulates endothelial transcriptional and post-transcriptional programs, priming the endothelium for later cytokine activation. Lipid accumulation also stimulates vascular smooth muscle cells (VSMC) and endothelial cells to generate inflammatory mediators and cytokines, contributing to the initial steps of the atherosclerotic process. These changes increase endothelial damage and impair endothelial healing. Endothelial cell activation induces the expression of leukocyte adhesion molecules, such as endothelial-selectin (E-selectin), P-selectin, and the glycoproteins intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1). This is followed by the production of chemokines, such as monocyte chemoattractant protein-1 (MCP-1), which stimulates monocyte migration and infiltration through its receptor C-C chemokine receptor 2 (CCR2). Similarly, interleukin (IL)-8 and fractalkine promote cell migration through C–X–C chemokine receptor type 2 (CXCR2) expressed on leukocytes. Infiltrating monocytes mature into macrophages in response to macrophage colony-stimulating factor (M-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF). LDLs are modified by oxidation (oxLDL), enzymatic processing, desialylation and aggregation. Macrophages differentiate into foam cells after recognizing and internalizing oxLDLs via an array of scavenger receptors, including scavenger receptor class A (SR-A), CD36, lectin-like oxidized LDL receptor-1 (LOX-1), scavenger receptor for phosphatidylserine and oxidized lipoprotein (SR-PSOX), and scavenger receptor class B type 1 (SR-B1). Moreover, oxLDLs, acting as DAMPs, stimulate TLRs in macrophages, aggravating inflammation in the plaque. Cholesterol efflux from macrophages is regulated by ATP binding cassette transporter A1 (ABCA1). Therefore, macrophages in the plaque show abnormal lipid metabolism with reduced cholesterol efflux, increased cell death, and reduced efferocytosis, leading to an inflammatory state Figure 2.

4OxLDLs also function as immune antigens. DCs and other APCs process intraplaque oxLDLs and stimulate the adaptive immune response by presenting oxLDL-derived antigens in atheromatous plaques and in secondary lymphoid organs. Consequently, CD4+ and CD8+ T cells are present in the plaque almost as early as monocytes and play essential roles in its development. The inflammatory response in the atherosclerotic lesion is also modified by infiltrating B cell subsets.

5After these initial steps, plaques progress to advanced lesions, composed of lipid droplets, foam cells, macrophages, and lymphocytes. These cells produce a plethora of cytokines and mediators with important roles in atherosclerotic progression. Smooth muscle cell growth and the production of collagens, matrix metalloproteinases (MMPs), fibronectin, and elastin also contribute to plaque development. Among other cell types, macrophages can stimulate production of MMPs that destabilize the plaque by stimulating the production of proinflammatory cytokines. Moreover, in advanced plaques, smooth muscle cells, macrophages, and foam cells undergo apoptosis and necrosis, leading to the formation of the necrotic core. Local inflammation in the intima stimulates inflammation in other vessel layers by systemic inflammation in other organs, including adipose tissue and the liver.

4.1. Monocytes

6The mononuclear phagocytic system consists of circulating monocytes, monocyte-derived DCs and macrophages, resident macrophages, and DCs. These cells participate in scavenging, inflammation, and anti-pathogen defenses, both in the direct response to foreign agents and in shaping each diverse phase of the inflammatory response. Circulating monocytes, which originate in the bone marrow, are generally found in blood, bone marrow, and the spleen in healthy animals. Circulating monocytes and resident vascular macrophages are the first leukocytes to be recruited to the early atheromatous plaque. Local inflammation is initiated by damaged endothelial cells, which release MCP-1 (also known as C–C motif chemokine ligand 2 (CCL2)). MCP-1 interacts with C–C chemokine receptors (CCR)2 and CCR4 expressed on circulating monocytes, recruiting them to the lesion. Monocyte recruitment also depends on other cytokines and chemokines, including IL-8, CCL3, CCL4, and CCL5.

7Several monocyte subsets are recruited to the atheromatous plaque, with the most common subset in mice being lymphocyte antigen 6 complex high (Ly6Chi) monocytes. In humans, the most prevalent monocytes in the plaque are CD14+CD16- cells, known as classical monocytes. CD14+CD16− and Ly6Chi monocytes both express CCR2. CD14+CD16− monocytes have a proinflammatory phenotype, and their number is increased in hypercholesterolemic conditions. Human atherosclerotic plaques also contain CD14+CD16hi monocytes (nonclassical) and CD14hiCD16+ monocytes (intermediate). Activated CD14hiCD16+ monocytes produce large amounts of proinflammatory molecules, such as tumor necrosis factor (TNF) α, and have been implicated in atherosclerotic progression. Recruited monocytes are an important systemic source for renewal of tissue macrophages and DCs, but they are not the only source of plaque monocytes, which can also originate from a local proliferation of monocytes and resident macrophages that maintain their capacity to mature and reach a phagocytic phenotype. Apart from their role as macrophage and DC precursors in atherosclerotic plaques, monocytes can trigger and modulate T-cell responses, regulate angiogenesis, and exert effector functions as accessory cells in atherogenesis. Increased numbers of circulating proinflammatory monocytes have been found in mouse models of atherosclerosis, such as ApoE−/− mice. Similarly, a high number of intermediate CD14hiCD16+ circulating monocytes seems to be related to increased atherosclerotic risk in unstable angina patients, and upregulation of TLR-4 on intermediate CD14hiCD16+ monocytes is associated with coronary plaque vulnerability in patients with angina pectoris.

8In mice, circulating monocytes are recruited to the subendothelial space by P and E-selectin-mediated tethering and rolling and ICAM1 and VCAM1-mediated adhesion. Knockdown of VCAM-1 or its inhibition with the antioxidant AGI-1067 results in reduced atherosclerosis in LDLR−/− mice.

9Monocyte migration to the subendothelial space depends on signaling via CCR2, CCR5, and CX3C-chemokine receptor 1 (CX3CR1). A blockade of these receptors decreases monocyte recruitment and reduces atheromatous plaque size in ApoE−/− mice. Monocyte recruitment and subsequent atherosclerosis in ApoE−/− mice are also reduced by inhibiting the chemoattractants CCL2, CXCR1, CCR5, and M-CSF, either by pharmacological blockade or genetic inactivation. Migrated monocytes differentiate into macrophages that contribute to inflammation and plaque development. In the course of hematopoiesis, the differentiation of monocytes into macrophages is triggered by M-CSF and GM-CSF. Circulating monocytes differentiate in response to stimuli such as inflammation and infection, with inflammation playing an essential role in atherosclerotic development.

4.2. Macrophages

10The early stages of atherosclerosis are characterized by the formation of fatty streaks, and these early lesions contain many macrophages. Macrophages in atherosclerotic plaques maintain local inflammation by producing reactive oxygen species (ROS) and secreting inflammatory cytokines and chemokines, including TNF-α, IL-1β, IL-6, IL-8, and TGF-β, which promote chemotaxis of B and T-cells and macrophages toward the plaque. Intraplaque macrophages have a reduced migratory capacity, acting instead to maintain inflammation and support plaque progression. Monocytes enter into the arterial intima and differentiate to macrophages but proliferation of artery wall macrophages has been associated with increased plaque development in advanced atherosclerotic lesions. Macrophages in lesions internalize and accumulate lipoproteins, converting to foam cells filled with lipid droplets. The accumulation of foam cells drives plaque growth. All phases of atherosclerosis are characterized by macrophage apoptosis and necrosis, which lead to the formation of the necrotic core in progressing plaques. This exacerbates the accumulation of inflammatory cells and impairs the removal of dead cells (efferocytosis), further increasing plaque size and instability.

11Macrophages are highly plastic, a property that allows them to hone responses to the specific microenvironment. Moreover, plaque composition and macrophage polarization are interdependent, each influencing the each other. Differentiation of recruited monocytes into macrophages in the plaque is determined by several factors, including the local microenvironment, macrophage metabolic state, gut microbiota-derived metabolites, and genetic and epigenetic factors.

12The classical classification of macrophages envisions two phenotypes, M1 and M2. Monocytes give rise to M1 or M2 macrophages in response to exposure to GM-CSF or M-CSF, respectively, and the predominance of M1 or M2 macrophages in atherosclerotic lesions has been proposed to reflect local M-CSF and GM-CSF concentrations. Complete M1 macrophage differentiation is achieved after exposure to Th1 cytokines, including TNFα and interferon (IFN)-γ, produced upon lipopolysaccharide recognition by TLR or lipoproteins.

13M1 macrophages are considered proinflammatory cells due to their capacity to secrete abundant proinflammatory factors, such as TNF-α, IL-1α, IL-1β, IL-6, IL-12, IL-18, IL-13, and IL-23, and the chemokines CXCL9, CXCL10, and CXCL11. Proinflammatory macrophages also produce ROS and nitric oxide (NO).

14M2 (or alternatively polarized) macrophages can be further divided into four different subsets, M2a, M2b, M2c, and M2d, depending on the activating stimulus. The M2a subset is induced by exposure to the Th2 cytokines IL-4 and IL-13 and expresses high levels of the mannose receptor (CD206) and IL-1 receptor agonist (IL1RN). These cells secrete the anti-inflammatory cytokines IL-10, IL-1, and TGF-β and profibrotic factors, such as fibronectin, that contribute to tissue remodeling. M2b macrophages are induced by immune complexes, TLR agonists, and IL-1 receptor agonist. M2c macrophages are induced by glucocorticoids, TGFβ, and IL-10 and produce the anti-inflammatory molecules pentraxin-3 (PTX3), TGFβ, IL-10, and Mer receptor kinase (METK). M2c macrophages are responsible for the removal of apoptotic cells. M2d macrophages differentiate in response to TLR signaling via the adenosine A2A receptor; these cells produce large amounts of IL-10 and vascular endothelial growth factor (VEGF) and promote angiogenesis in tumors and atherosclerotic plaques. M2 macrophages, with the exception of the M2b subset, produce large quantities of anti-inflammatory cytokines, such as IL-10.

15Atherosclerotic lesions also contain other macrophage phenotypes. Mox macrophages are inflammatory cells that lack CD163 expression and show reduced phagocytic and chemotactic abilities and an elevated capacity for TLR-2-dependent production of IL-1β and cyclooxygenase-2 (COX-2) in an oxLDL-rich microenvironment. Mox macrophages account for almost a third of the total macrophage content of advanced atherosclerotic plaques in mice and play an antioxidant role dependent on their overexpression of Nrf2-related genes, such as heme oxygenase-1 (HMOX-1), sulforedoxin-1, and thioredoxin reductase. Mox macrophages were initially described only in mouse models of atherosclerosis but have since been identified in humans.

16Blood vessel injury releases erythrocytes and iron-holding pigments, which can be phagocytosed by macrophages. Human atherosclerotic plaques in which neovascularization takes place contain iron deposits that can trigger the differentiation of M(Hb) macrophages (also known as Mhem). M(Hb) macrophages express the scavenger receptor cysteine-rich type-1 protein M130 (CD163) and macrophage mannose receptor 1 (MMR, known as CD206), along with heme-dependent activating transcription factor 1 (ATF1) which induces expression of heme oxygenase 1 and liver X receptor β (LXR-β). The expression of the LXR-β-dependent genes LXR-α and ABCA1 by this macrophage subtype increases cholesterol efflux, and M(Hb) macrophages have an antiatherogenic role related to their low lipid-loading capacity and anti-inflammatory properties, mediated through the production of IL-10 and apolipoprotein E.

17M4 macrophages are produced by stimulation with the chemokine C–X–C motif chemokine 4 (CXCL4) and play a proatherogenic role through the production of MMP12 and the promotion of plaque instability. M4 macrophages have a lower capacity for phagocytosis than M1 and M2 macrophages and limit the generation of Mhem macrophages. Another intraplaque macrophage subtype is the IL-17A-stimulated macrophage.

18Macrophages play decisive roles at all stages of atherosclerotic lesion progression, and intraplaque macrophage subtypes are heterogeneous. Both M1 and M2 macrophages are found in atherosclerotic lesions, with M1 macrophages found in the lesion shoulder, which is the least stable region of the plaque, while both M1 and M2 macrophages are found in the fibrous cap, close to the necrotic core. The production of proinflammatory factors by M1 macrophages results in inflammatory cell recruitment, accelerated plaque development, and increased necrotic core formation and plaque vulnerability, leading to thrombotic events. In contrast, M2 macrophages play an anti-inflammatory and atheroprotective role through the inhibition of cell recruitment and tissue remodeling. M2 macrophages also reduce foam cell formation and increase plaque stability. The proinflammatory and anti-inflammatory intraplaque macrophage content can, thus, serve as an index of plaque progression/instability or regression.

19LDLs induce proinflammatory macrophage polarization by increasing the production of TNFα and IL-6 and reducing the expression of the anti-inflammatory M2 markers CD206 and CD200R. Modified LDLs promote a stronger proinflammatory phenotype in macrophages upon recognition by TLRs and scavenger receptors like CD36. OxLDLs also promote a switch in macrophage phenotype from M2 to M1.

20Some studies suggest that atherosclerosis’s development might be influenced by macrophage polarization in non-arterial tissues, as described in the epicardial adipose tissue of patients with coronary artery disease.

4.3. Foam Cells

21Accumulation of lipoproteins in the arterial intima is a key element in the onset and development of atherosclerosis. Lipoproteins with a diameter below 70 nm include high density lipoproteins (HDL), LDL, intermediate-density lipoproteins (IDL), most very low-density lipoproteins (VLDL), and some chylomicrons, and these biochemical assemblies can cross the endothelium from the blood and enter the arterial intima, where they are modified by oxidizing agents, proteases, and lipases, generating oxLDLs, acetylatedLDLs, etc. Modification of LDLs also induces their aggregation. These aggregated and modified LDLs can be internalized by VSMCs, DCs, and especially by macrophages, triggering their conversion to foam cells.

22Lipid metabolism in macrophages depends on cholesterol uptake, esterification, and efflux. An imbalance among these processes results in the formation of lipid-dense macrophages, called foam cells, and most foam cells are derived from macrophages with a disproportionate influx of modified LDLs and cholesterol esters. However, a small fraction of foam cells originate from VSMCs and endothelial cells. Monocytes are also important in foam cell formation. Macrophages internalize modified or native LDLs after binding by scavenger receptors; eight proteins able to bind modified lipoproteins have been described in macrophages, the best described being SR-A1, CD36, and LOX-1. Scavenger receptors can be modulated by MEKK-2, MAP kinase, and STA. Macrophages generate cholesterol esters through the action of acyl-coenzyme A: cholesterol acyltransferases (ACATs). Lipoprotein uptake and cholesterol ester generation are balanced in homeostatic conditions by the hydrolysis of cholesterol esters to free fatty acids and of cholesterol by neutral cholesteryl ester hydrolase 1 (NCEH1) and lysosomal acid lipase (LAL). Cholesterol efflux is mediated by ABCA1, ATP-binding cassette sub-family G member-1 (ABCG1), and scavenger receptor SR-B1. In disease conditions, this balance is disrupted by the increased macrophage expression of LOX-1 induced by proinflammatory cytokines and by the high levels of oxLDL, accompanied by decreased expression of ABCA1 and ABCG1. These changes result in the intracellular accumulation of cholesterol and the generation of foam cells. Foam cells have less proinflammatory capacity than M1 macrophages in response to the M1-polarizing factors LPS and IFN-γ. In contrast, foam cells develop an anti-inflammatory response similar to M2 macrophages in response to the M2-polarizing signal IL-4. Indeed, foam cell accumulation in M1-polarizing plaques results in attenuation of macrophage-associated inflammation.

23Increased LOX-1 expression in atherosclerosis is also observed in endothelial cells, leading to PKC activation. Subsequent activation of RhoA/Rho kinase and protein phosphatase 1 regulatory subunit 14A (PPP1R14A) leads to occludin phosphorylation and cytoskeketal rearrangement, respectively. LOX-1 overexpression reduces the expression of the desmosome components desmoglein 1 (DSG1) and desmocollin 2 (DSC2), downregulating desmosomal intercellular contacts. Through these mechanisms, atherosclerosis-induced LOX-1 overexpression impairs intercellular interactions, promotes endothelial permeability to oxLDL and its access to the subendothelial space, and enhances foam cell formation.

24OxLDL and other modified LDLs are internalized by altered phagocytosis. SR-A1 exists in three isoforms. The full-length SR-A1 and shorter SR-A1.1 isoforms are encoded by the MSR-1 gene and participate in oxLDL recognition and internalization, whereas the lipid-transport-dysfunctional SR-A1.2 isoform acts as an inhibitor of the other two isoforms. SR-A1 and SR-A1.1 have high affinity for acetylated LDL and oxLDL. The knockout of SR-A1 in ApoE−/− and LDLR−/− mice inhibits foam cell formation and reduces atherosclerosis. A similar reduction in atherosclerosis is observed in MSR-1−/−, ApoE−/−, and MSR-1−/− LDLR−/− mice. Total or macrophage-specific deletion of SR-As results in fewer atherosclerotic lesions. SR-A1 expression is upregulated by proinflammatory cytokines via NFκB and is downregulated by polyphenols via inhibition of peroxisome proliferator-activated receptor γ (PPARγ) and by curcumin via calpain-associated ubiquitination and degradation.

25CD36 is a member of the B family of scavenger receptors. OxLDL-dependent CD36 production regulates inflammation through the induction of the TLR4/TLR6 complex assembly, NFκB activation, and chemokine release. Accordingly, CD36 deficiency in macrophages diminishes cytokine production. CD36 inhibition reduces oxLDL content in the arterial wall.

26In macrophages, CD36 levels can be upregulated by curcumin-induced expression of nuclear factor (erythroid-derived 2)-like 2 (NFE2L2), whereas in monocytes, CD36 is increased by LPS via upregulation of AP-1 transcription factors and by palmitate. CD36 can be inhibited by ceramides in monocytes and by plant antioxidant in macrophages. CD36 knockout in ApoE−/− mice protects against atherosclerotic lesion development only in males. In contrast, CD36−/−-ApoE−/− females show a relative increase in the number of atherosclerotic lesions.

27LOX-1 is highly expressed in atherosclerotic plaques in humans and in macrophages during atherosclerosis, accounting for 40% of oxLDL internalization. LOX-1 is induced in macrophages by proinflammatory cytokines, oxLDL, LPS, advanced glycation end-products, and ROS. In mouse models of atherosclerosis, LOX-1 knockout decreases disease and inflammation, whereas LOX-1 overexpression has the opposite effect.

28The accumulation of cholesterol esters in macrophages leads to the generation of foam cells. The transformation of cholesterol to cholesterol esters is catalyzed by acetyl-CoA acetyltransferase (ACAT1), and the reverse process is mediated by NCEH.

29Atherosclerosis in LDLR−/− mice is aggravated by macrophage-restricted depletion of ACAT1. In contrast, systemic ACAT1 deficiency ApoE−/− and LDL−/− mice does not affect atherosclerosis, but these mice develop dermal xanthomas and form cholesterol deposits in the brain. Pharmacological inhibition of ACAT1 increases plaque formation in mouse and rabbit models of atherosclerosis. ACAT1 activity or expression can be modulated by several molecules, such as the non-specific inhibitor F-1394, the intestinal hormone Ghrelin via PPARγ, protein kinase A (PKA) via incretin hormones, dipeptidylpeptidase 4 (DDP4) via the incretin hormone glucagon-like peptide-1 (GLP-1), insulin via CCAAT/enhancer-binding protein α (C/EBPα) and extracellular signal-regulated kinase (Erk), p38MAP kinase, Jnk, and leptin via janus-activated kinase 2 (Jak2)/phosphatidylinositide 3-kinase (PI3K).

30NCEH hydrolyzes cholesterol esters to release free cholesterol that can be exported from the cell. In mouse models, NCEH inhibition increases atherosclerosis, whereas NCEH overexpression diminishes the lesion’s necrotic core. NCEH overproduction in macrophages also reduces cholesterol esters. The NCEH1 isoform accelerates atherosclerosis in ApoE−/− mice. NCEH and NCEH1 inhibit foam cell generation.

31Cholesterol efflux is mediated by the transporters ABCA1 and ABCG2 and the scavenger receptor SR-B1, and by passive membrane diffusion with simultaneous genetic disruption of ABCA1; and SR-B1 potentiates foam cell formation but has no effect on lesion development. In LDLR−/− mice, ABCA1 overexpression in the liver leads to the accumulation of proatherogenic LDL and enlarged aortic atherosclerotic lesions.

32The effect of ABCG1 deletion is antiatherogenic or moderately proatherogenic, depending on the study. SR-B1 overexpression has an atheroprotective effect, whereas its deletion produces a proatherogenic phenotype, demonstrating the antiatherogenic role of SR-B1.

33ABCA1 is regulated by transcription factor liver X receptor α (LXRα), the flavonoid quercetin via the PPARγ/LXRα pathway, proteasome inhibition, and ApoA-1. Foam cell formation is reduced by ABCA1 upregulation by C–X–C motif chemokine 5 (CXCL5), as well as cAMP, sterols, and PPARγ agonists. ABCA1 expression is negatively regulated by unsaturated free fatty acids via PKCδ-dependent phosphorylation and by IL-12 and IL-18 via activation of the zinc finger protein ZNF202. Macrophage ABCA1 and ABCG1 can be upregulated by the monoterpenoid cineol and by olive-oil. ABCA1 and ABCG1 levels are increased by the gut microbiota metabolite—protocatechuic acid (PCA), acting via miR-10b. ABCG1 and SR-B1 levels are increased by caffeic and ferulic acids. LXRα and SR-BI are enhanced by resveratrol and 13-hyroxy linoleic acid via PPARγ. ABCA1, ABCG1, and SR-B1 are reduced via LXRα by the metalloproteinase pappalysin-1 (PAPPA), which hydrolyzes insulin-like growth factor-binding proteins (IGFBP).

34The accumulation of cholesterol crystals provokes the production of pro-inflammatory cytokines by M1 macrophages via the caspase-1-activating NLRP3 inflammasome. Moreover, cholesterol esters induce the M1 phenotype by activating TLR4 and inducing the NF-κβ pathway. A major product of cholesterol ester oxidation, 9-oxononanoyl-cholesterol, increases the release of TGF-β and promotes the generation of anti-inflammatory macrophages. In addition, conjugated linoleic acid promotes M2 polarization by augmenting IL-10 production

4.4. Dendritic Cells

35DCs link the innate and adaptive immune systems by presenting antigens to T cells. Immature DCs patrol tissues under physiological conditions. Upon activation, maturing DCs increase the expression of MHC class II (MHCII) and the costimulatory molecules CD80, CD86, and CD83 and migrate to draining lymph nodes, where they stimulate the adaptive immune response by priming T cells and secreting cytokines. Key features of DCs include stellate morphology, high expression of MHCII, and the capacity to take up, process, and present antigens, such as those derived from apolipoproteins.

36Several DC subsets derive from a specific precursor population of common dendritic progenitors (CDP). CDPs give rise to plasmacytoid DCs (pDCs) in bone marrow or generate pre-DCs that circulate in blood and give rise to classical DCs (cDCs) in lymphoid and non-lymphoid organs. cDCs can be classified as cDC1 and cDC2. pDCs and cDCs are induced by the growth factor fms-like tyrosine kinase 3 ligand (Flt3L). DCs can also originate from circulating monocytes after their migration to tissues, where they differentiate to macrophages or monocyte-derived DCs through the action of M-CSF or GM-CSF, respectively; these monocyte-derived DCs are considered part of the mononuclear phagocyte system (MPS). Monocyte-derived DCs express CD11c and MHCII, and these markers have been widely used in studies of the role of DCs in atherosclerosis; however, some monocytes and macrophages also express these markers. Following the nomenclature used by other authors, herein we refer to CD11c+MHCII+ DCs as APCs, and use pDC and cDC for more specific DC populations.

37During atherosclerosis, endothelial cells enter a state of chronic activation, leading to the recruitment of monocytes into the subendothelial intima. Conditions in the intraplaque microenvironment trigger the generation of monocyte-derived DCs. The role of these DCs in atherosclerosis is unclear. A proatherogenic role in the early phases of atherosclerosis has been proposed, as has as an atheroprotective function.

38CD11c+MHCII+F4/80− APCs have been detected in atherosclerosis-prone areas of the mouse aorta before lesions develop. CD11c+ APCs migrate from atherosclerotic plaque upon blockade of CCL19 and CCL21, in a process dependent on CCL7. CD11c+MCHII+ DCs have been found in atheromatous plaques in mice containing Flt3-dependent CD103+ and CD11b+ CD172a+ cDCs and monocyte-derived CD11b+ DCs, both of which are M-CSF-dependent and CD64-expressing. In the early stages of plaque formation, CD11c+ APCs can take up lipids and contribute to foam cell formation. DCs in advanced atherosclerotic lesions show the activation of markers, including the costimulatory molecules CD83 and CD86 and cytokines.

39Antigen presentation by DCs has been described in secondary lymphoid organs and in the atheromatous plaque. Isolated aortic CD11c+MHCII+ APCs induce T cell proliferation in vitro and stimulate T cell production of TNF-α and IFN-γ. The importance of antigen presentation by APCs in atherosclerosis has been revealed by several studies. In LDLR−/− mice, abrogation of the invariant chain of CD74, a protein involved in MHCII-peptide complex formation, reduces T cell activation and atherosclerosis; however, in ApoE−/− mice, the inability to present antigens on MHCII increases atherosclerosis by reducing the pool of atheroprotective Tregs and increasing proatherogenic CD8+ T cells. The reason for this discrepancy is unknown, but an atheroprotective role of antigen presentation via MHCII is supported by the finding that TLR-activated CD11c+ DCs promote Treg development and function in association with increased atherosclerosis. Additionally, a cDC-specific loss of MHCII causes colitis and reduced Treg activation. Atherosclerosis is also affected by the modulation of other key molecules in DCs’ function. Lack of TGFβ type II receptor signaling in CD11c+ APCs promotes atherosclerosis in ApoE−/− mice. Loss of (HIF)-1α in CD11c+ APCs in LDLR−/− mice increases proatherogenic T cell infiltration and the expansion of atherogenic Th1 cells. The ablation of MyD88, a TLR adaptor, in CD11c+ APCs produces a reduction in Tregs. Abrogation of the mechanosensitive Kruppel-like factor 2 (KLF2) in CD11c+ APCs promotes surface localization of the costimulatory molecules CD40 and CD86 and increased T cell proliferation and apoptosis. After Klf2−/− bone marrow transplant to LDLR−/− mice, the absence of KLF2 increases the number of DCs in lesions, enhances T cell activation and cytokine production, and increases atherosclerotic lesions’ size. APCs also mediate tolerogenic responses by reducing effector T cell functions and enhancing Treg functions. In LDLR−/− mice, oxLDL-loaded, bone–marrow-derived DCs reduce atherosclerotic lesion size by inhibiting the Th1 response, while ApoB100-loaded, bone–marrow-derived DCs achieve the same effect by increasing Treg responses.

4.4.1. cDCs

40Investigation of the role of cDCs in atherosclerosis has yielded conflicting results. Atherosclerotic plaque size is unaffected in LDLR−/− mice, reconstituted with bone marrow depleted of cDCs by the insertion of diphtheria toxin receptor (DTR) into the cDC-specific Zbtb46 locus. However, CD103+ DC depletion in LDLR−/−Flt3−/− mice shows the depletion of aortic Tregs and increased atherosclerosis. Plaque size is unaffected in LDLR−/− mice reconstituted with Baft3−/− bone marrow and in LDLR−/−Batf3−/− mice. However, experiments in ApoE−/− Batf3−/− mice support a proatherogenic role and elevated Th1 stimulation capacity for Batf3-dependent DCs. These disparities likely reflect the different mouse models used. A proatherogenic function has been described for DNGR1+ CD8α+/CD103+ DCs.

4.4.2. pDCs

41Depletion of pDCs in atherosclerotic mouse models has been achieved using a number of antibodies against bone marrow stromal cell antigen 2 (BST2), resulting in enhanced atherosclerosis in LDLR−/− mice and reduced atherosclerosis in ApoE−/− mice. Injection of diphtheria toxin (DT) to deplete pDCs in LDLR−/− mice, reconstituted with γ-irradiated BDCA2-DTR bone marrow, results in increased atherosclerosis. In contrast, atherosclerosis is unaffected in DT-treated ApoE−/− BDCA2-DTR mice.

42An atheroprotective effect was found upon CD11c-specific deletion of the transcription factor E2-2/Tcf4 in pDCs or impairment of MHCII antigen presentation in pDCs, indicating a proatherogenic role of pDCs in MHCII-dependent antigen presentation via T cell responses in atherosclerosis.

43Human studies suggest a correlation between low circulating levels of cDCs and pDCs and peripheral artery disease, and DC accumulation and activation is associated with plaque vulnerability.

4.4.3. Regulatory DCs

44Regulatory DCs can present antigens but express low levels of costimulatory molecules and proinflammatory cytokines, while expressing higher levels of anti-inflammatory cytokines; moreover, regulatory DCs are refractory to maturation signals. Regulatory DCs promote immune tolerance by reducing the expression of costimulatory molecules, increasing the expression of inhibitory molecules, such as indoleamine 2,3-dioxygenase (IDO), inhibiting the production of the proinflammatory cytokines IL-12 and TNFα, and promoting the induction of the anti-inflammatory cytokines IL10 and TGFβ. Regulatory DCs mediate depletion and anergy of proinflammatory effector T cells and the generation and expansion of atheroprotective Tregs.

45Self-antigen recognition plays an important role in the chronic inflammation associated with atherosclerosis. The accumulation of native LDLs, oxLDLs, and apolipoprotein B100 (ApoB100) in the vessel wall attracts immune cells and triggers chronic inflammation. The loading of DCs with oxLDL and ApoB100 diminishes the generation of proinflammatory cytokines and promotes the production of Tregs.

46DC tolerance is generated by anti-inflammatory molecules, such as IL-10 and TGFβ, and immunosuppressive enzymes, such as IDO. Adoptive transfer of oxLDL-loaded DCs exacerbates atherosclerosis, while intravenous transfer of tolerogenic ApoB100-loaded and IL10-treated DCs attenuates atherosclerosis in hypercholesterolemic LDLR−/− mice expressing human ApoB100.

47Apoptotic cells are removed through efferocytosis, and the impairment of this process in atherosclerotic plaques increases inflammation. Intravenous administration of oxLDL-induced apoptotic DCs to LDLR−/− mice reduces atherosclerosis and increases plaque stability by increasing CD103+ tolerogenic DC and Treg numbers and reducing the numbers of Ly6Chi monocytes and the level of circulating CCL12. Further studies are needed to determine the role of tolerogenic DCs in atherosclerosis’s onset and development.

5. Adaptive Immunity

48Adaptive immunity is a highly precise and lifelong immune response that plays essential roles in distinguishing foreign from self-antigens. Adaptive immunity is mainly mediated by T and B cells, which precisely recognize antigens through the specific receptors expressed on their surfaces, the T-cell receptor (TCR) and B-cell receptor (BCR).

49T cells are classified according to membrane and intracellular markers. They express the αβ or γδ TCR, CD3, and one of the coreceptors CD4 or CD8. The TCR-CD3 complex recognizes antigens presented in the context of major histocompatibility complex molecules (MHC or human leukocyte antigen (HLA) in humans) by an APC.

50B cells produce antibodies, act as APCs, and release cytokines. B cells are categorized according to the expression of the cell-lineage marker CD19 and a variety of surface and intracellular proteins; the distinct BCRs they express; and their production of antibodies and cytokines.

51APCs are able to present antigens to cognate naïve CD4+ and CD8+ T cells. These antigens include non-self-antigens and self-antigens, including ox-LDLs and heat shock protein 60 (HSP 60). Upon activation, CD4+ T cells proliferate and differentiate into specialized effector T helper (Th) cells, whereas activated CD8+ T cells proliferate and differentiate into CD8+ cytotoxic T lymphocytes (CTL). Naïve CD4+ T cells can differentiate into various cell subsets, including effector T cells (T helper 1 (Th1), Th2, and Th17) and regulatory T cells (Treg). T-cell differentiation into varied Th subsets depends on the type of antigen encountered, the TCR signal intensity, and the local cytokine milieu. These factors mediate Th polarization in atherosclerotic lesions.

5.1. CD4+ T Cell

52Th phenotypes are classified by the differential expression of surface molecules, transcription factors, and effector cytokines. Th1 cells are characterized by the release of large amounts of IFN-γ and IL-2 and the expression of the master transcription factor T-bet. Th2 cells produce IL-4, IL-5, and IL-13 and express the master transcription factor GATA-3. Th17 produce the cytokine IL-17 and express the transcription factor RORγt. Tregs are defined by the expression of the transcription factor forkhead box 3 (Foxp3) and the extracellular marker CD25.

53Although macrophages account for most inflammatory cells in atherosclerotic lesions, T and B cells play an essential role in atherosclerotic plaque development through by their capacity to control immune responses during disease onset and progression. Atherosclerotic plaques have been found to contain CD4+ and CD8+ T cells, B cells, NKT cells, and follicular helper T cells. T cells account for 10% of all cells in human plaques, with 70% of them being CD4+ T cells and most of the remaining 30% being CD8+ T cells. The most abundant CD4+ T cells in the plaque are Th1 cells, but Th2, Treg, and Th17 cells have also be found, as have TCRγδ+ T cells and NKT cells.

54Global CD4+ T cell abrogation in ApoE−/− mice confers atheroprotection, whereas plaque size is increased by adoptive transfer of CD4+ T cells from ApoE−/− mice or modified-LDL-reactive CD4+ T cells. However, the total abrogation of CD4+ T cells results in the absence of proinflammatory and anti-inflammatory cell populations with opposite influences on atherosclerosis.

5.1.1. Th1

55Th1 cells play a proatherogenic role in atherosclerosis. OxLDLs increase antigen presentation by DCs through HSP60, enhancing T-bet expression, Th1 polarization, and IFN-γ production. Moreover, activated macrophages in atherosclerotic lesions produce IL-12 and IL-18, which also induce Th1 polarization and IFN-γ production. The IL-12–IL-18–T-bet–IFN-γ pathway is a powerful proinflammatory stimulus that promotes and accelerates lesion development, and atherosclerosis is reduced by disruption of the IL12 gene in ApoE−/− mice or by functional blockade of IL-12 with anti-IL-12 antibodies, accompanied by increased plaque stability, as indicated by augmented collagen levels. Atherosclerosis in ApoE−/− mice is also reduced and plaques are stabilized by IL-18 blockade with an IL-18 binding protein or by genetic deletion.

56The Th1 lineage-specific transcription factor T-bet, a member of the of the T box family, promotes Th1 differentiation by binding to the IFN-γ promoter, stimulating IFN-γ production. T-bet deficiency slows atherosclerosis development and increases production of the atheroprotective Th2 cytokines IL-4, IL-5, and IL-10, and IgM antibodies. T-bet also promotes atheroprotection in cooperation with Foxp3 by increasing Treg activity.

57Th1 cells produce high levels of IFN-γ. IFN-γ promotes plaque development, as shown in ApoE−/− mice by the proatherogenic effect of recombinant IFN-γ injection and the atheroprotective effect of Ifng gene knockout. IFN-γ stimulates the IFN-γ cell surface receptor complex (IFN-γR), activating janus kinases (JAK) and recruiting and activating STAT1 (signal transducer and activator of transcription 1), which translocates to the nucleus and stimulates the transcription of IFN-γ target genes, such as MCP-1 and ICAM-1. Inhibition of STAT1’s activity in LDLR−/− mice is atheroprotective, confirming the importance of the IFN-γ–JAK–STAT1 pathway during lesion progression. IFN-γ modulates the recruitment of immune cells by inducing endothelial cell expression of ICAM-1 and VCAM-1 and by promoting foam cell formation through the modulation of key genes involved in cholesterol metabolism, including ABCA1 and ACAT1, and SR-A and SR-SPOX. IFN-γ also stimulates CCR5 production in atherosclerosis.

58The proatherogenic effect of Th1 cells in atherosclerosis appears to involve an important role for the chemokine receptor CCR5, a well-known HIV-1 co-receptor, through the T cell recruiting action and other effects of its ligands: macrophage inflammatory protein 1α (MIP-1α, CCL3), MIP-1β (CCL4), and RANTES (regulated on activation normal T cell expressed and secreted, CCL5). The naturally-occurring human variant CCR5delta32 downregulates CCR5 gene function. The CCR5delta32 allele has been linked to protection against coronary artery disease and heart disease and a lower risk of myocardial infarction. However, this protective effect has not been observed in other studies in diverse populations. Mouse studies show that CCL5 receptor antagonism and genetic depletion exacerbate atherosclerosis. The CCR5 blocking antibody maraviroc has been used in HIV patients to block viral entry to CD4 T cells. CCR5 blockade with this antibody also reduces atherosclerosis in mouse models and HIV patients. Deletion of CCL5 in ApoE−/− mice reduces atherosclerosis in a CCR5-dependent-manner, and in [44AANA47]-RANTES, which prevents CCL5 ligation with glycosaminoglycans, reduces atherosclerosis, and increases plaque stability in LDLR−/− mice. In addition, disruption of TGF-β signaling in CD4+ T cells of ApoE−/− mice promotes atherosclerosis by enhancing the Th1 response.

5.1.2. Th2

59Th2 differentiation is triggered by IL-4 via STAT6-induced GATA-3 expression. Th2 cells are characterized by the production of IL-4, IL-5, and IL-13 and the promotion of B cell-mediated responses. The role of Th2 cells in atherosclerosis remains controversial. An atheroprotective role is supported by the association of elevated numbers of circulating Th2 cells with less severe atherosclerosis and a lower risk of acute myocardial infarction in women. Moreover, Th2 cells counteract the proatherogenic effects of IFN-γ-producing Th1. The Th2 cytokines IL-5 and IL-3 appear to be atheroprotective through their capacity to augment collagen deposition, diminish monocyte recruitment, and potentiate M2 polarization. ApoB vaccination promotes Th2 responses that reduce atherosclerosis. However, experimental manipulation of the signature Th2 cytokine IL-4, which inhibits Th1 responses, has produced conflicting results. Adoptive transfer of IL-4−/− bone marrow to LDLR−/− mice significantly reduces atherosclerosis, but similar studies in IL4−/− plus ApoE−/− or LDLR−/− double knockouts showed no effect on atherosclerotic plaque development, and IL-4 administration provided no protection against atherosclerosis. Moreover, IL-4 increases a macrophage’s expression of the proatherogenic molecules CD36 and SR-A, and of VCAM-1, MMP1, and MCP1.

60Recent studies suggest that indirect modulation of the Th2 response is atheroprotective. MHCII−/−ApoE−/− double knockout mice show aggravated atherosclerosis and reduced levels of Th2 cytokines in plasma. Similarly, CCL1−/−ApoE−/− mice show increased atherosclerosis and an elevated splenocytic Th1:Th2 ratio, whereas IL-12p35−/−ApoE−/− mice show reduced atherosclerosis and a reduced Th1:Th2 ratio. Notably, these three mouse models all show a significant atheroprotective role of Tregs. In contrast, the Th2 response appears to aggravate atherosclerosis in an asthmatic ApoE−/− mouse model.

5.1.3. Th17

61Th17 cells have a role in the protection against extracellular pathogens. Th17 differentiation is induced by IL-6 and TGF-β, which mediate the activation of STAT3 and the production of the Th17 signature transcription factor retinoic acid-related orphan receptor γT (ROR γT). Th17 cells and their signature cytokines have been linked to autoimmune diseases and to atherosclerosis.

62Th17 cells are found in human atherosclerotic plaques but appear to have proatherogenic and antiatherogenic properties, possibly depending on animal model or methodological approach used and reflecting specific responses of Th17 cells to environmental cues. The pathogenic action of Th17 cells in atherosclerosis depends on their capacity to produce proinflammatory factors, such as IL-6, IFN-γ, and GM-CSF, and some pathogenic Th17 cells are derived from Tregs that lose FOXP3 expression and immunosuppressive properties.

63Th17 polarization is triggered by several cytokines. IL-23 enhances pathogenic and proinflammatory effects of Th17 cells in humans, and IL-23 blockade impedes Th17 cell production of IFN-γ and GM-CSF. Pathogenic Th17 cells are also potentiated by IL-1β and TGF-β3 and are differentiated into atheroprotective IL-10-producing cells by TGF-β1 in the intestine.

64Th17 cytokines play an important role in atherosclerosis. Th17 cells secrete IL-17A, IL-17F, IL-22, and IL-23. IL17 stimulates the NF-κB, ERK1/2, CCAAT/enhancer-binding protein β (C/EBPβ), and C/EBPδ signaling pathways. This induces the production of proinflammatory cytokines, including TNFα, IL-1β, IFN-γ, IL-6, IL-8, and GM-CSF in various target cells, such as endothelial cells, smooth muscle cells, macrophages, and Th1 cells.

65IL-17A can be produced not only by Th17 cells but also by CD8+ T cells, γδ T cells, invariant natural killer T cells (iNKT), NKT cells, natural Th17 cells, lymphoid tissue inducer (LTi) cells, group 3 innate lymphoid (ILC3) cells, macrophages, neutrophils, and mast cells. The role of IL-17A in atherosclerosis appears to be complex, with both proatherogenic and antiatherogenic roles reported. A proatherogenic role is supported by the capacity of IL-17A to induce VSMC production of proinflammatory factors, such as IL-6, CXCL8, and CXCL10, whereas an anti-inflammatory role is suggested by its ability to inhibit the action of VCAM-1 and adhesion molecules on fibroblasts and VSMCs and by its capacity decrease the production of proatherogenic IFN-γ.

66Several studies have reported that genetic abrogation of IL-17A or its receptor in atherogenic mouse models reduces atherosclerotic lesions and plaque vulnerability, supporting a proatherogenic role for IL-17. Another study showed that antibody blockade of IL-17A in ApoE−/− mice reduces plaque vulnerability. However, another study indicated that IL17A is atheroprotective and favors plaque stability in LDLR−/− mice. VSMC-dependent release of IL-17C plays a proatherogenic role by promoting the recruitment of proinflammatory IL-17A-expressing Th17 cells to atherosclerotic plaques.

67IL-22 is a member of the IL-10 family produced by Th17, Th22, cells, γδ T cells, NKT cells, and ILCs that has been linked to proinflammatory and anti-inflammatory roles. IL-22 has been detected in atherosclerotic lesions and reduces cholesterol efflux from macrophages by reducing the expression of the cholesterol efflux transporter ABCG1 and promotes the production of MMP-9 and the proinflammatory cytokines IL-1β, IL-6, and TNFα. IL-22−/−ApoE−/− mice show reduced plaque size and increased VSMC integrity. Intriguingly, IL-23 and IL-22 reduce atherosclerosis by repressing proatherogenic microbiota.

5.1.4. Tregs

68Tregs suppress a wide range of immune cells, including CD4+ and CD8+ T cells, B cells, and NKT cells and drive DCs and macrophages toward a more tolerogenic phenotype.

69Most Tregs express the master regulator of Treg development and function FOXP3, which is used as a marker for their identification. Natural Tregs (nTreg), which are generated in the thymus, mainly mediate tolerance to self-antigens through the expression of IL-10 and TGF-β. nTregs are positive for the markers FOXP3+CD4+CD25+. Inducible Tregs (iTregs) are prominently implicated in pathogen tolerance and are generated from naïve T cells in the periphery. iTregs may or may not express FOXP3 and present a variety of phenotypes, including Foxp3+Tregs; IL-10-producing T regulatory type 1 (Tr1) cells, which lack FOXP3 and CD25 expression; and TGF-β-producing T helper type 3 (Th3) cells. Th3 cells intervene in oral tolerance, express CD25 and Foxp3, and mediate suppression of Th1 and Th2 proliferation primarily by the release of TGF-β, but not IL-10.

70Treg cell generation and function is promoted by CD11c+CD103+ DCs and signaling from IL-10 and TGF-β. Tregs play an important role in the suppression of immune responses, self-tolerance, and homeostasis by regulating the immune balance.

71Tregs exert their immunoregulatory and suppressive activity through several mechanisms. One prominent mechanism is contact-dependent cell-mediated inhibition, and Tregs express suppressive surface molecules, such as T-lymphocyte–associated antigen-4 (CTLA-4) and programmed cell death-1 (PD-1). CTLA-4 downregulates APC function and T cell activation by diminishing CD80 and CD86 expression in the APC and by blocking the co-stimulatory interaction between CD80/CD86 in the APC and CD28 in the T cell. Tregs can mediate effector cell eradication by the production of granzyme B or by the generation of the tumor necrosis factor-related apoptosis inducing ligand (TRAIL)/death receptor 5 (DR5) and galectin-1, which promote effector T cell apoptosis. Tregs also secrete the immunosuppressive cytokines TGF-β, IL-10, and IL-35.

72FOXP3 expression and Treg generation and function are induced by TGF-β. TGF-β reduces plaque size and increases plaque stability by inhibiting the recruitment and activation of proinflammatory cells and by increasing VSMC numbers and promoting collagen accumulation. In ApoE−/− mice, disruption of TGF-β signaling enhances atherosclerosis, whereas TGF-β overexpression reduces atherosclerotic lesion vulnerability and atherosclerosis.

73IL-10 plays a protective role in atherosclerosis by inhibiting Th1 differentiation and decreasing T cell and macrophage accumulation and by diminishing the production of proinflammatory cytokines. In ApoE−/− mice, Tr1 cells, among other cell types, reduce inflammation and plaque lesions by producing IL-10 and reducing the generation of IFN-γ.

74IL-35, a member of the IL-12 cytokine family, binds to IL-35R and stimulates STAT1 and STAT4 in T cells and endothelial cells and STAT1 in B cells. IL-35 suppresses Th1 and Th17 cell proliferation and function while promoting Treg and regulatory B cell activity. IL-35 is found in atherosclerotic lesions, and its circulating level is reduced in stable angina pectoris patients. Treatment with IL35 reduces atherosclerosis in ApoE−/− mice.

75Nevertheless, the role of IL-35 is complicated by its sharing of subunits with other IL-12 family members, including subunit IL-12A with IL-12 and subunit EBI3 with IL-27. EBI3 deficiency in LDLR−/− mice reduces atherosclerosis, although other studies indicate a proatherogenic role for IL-27. Therefore, further studies are needed to define the role of IL-35 and IL-27 in atherosclerosis.

76Tregs mediate immunosuppression by disruption metabolism. Tregs deplete IL-2 from the media and express CD39 and CD73, which then hydrolyze extracellular ATP to produce pericellular adenosine. This adenosine activates the adenosine A2A receptor, which potentiates Tregs and inhibits effector T cell functions.

77Tregs are found in atherosclerotic lesions. ApoE−/− mice fed a hypercholesterolemic diet have fewer Tregs and more atherosclerosis than counterparts fed a normal diet. Atherosclerosis has been linked to a variety of Treg phenotypes. Several studies demonstrate a protective role for Treg subsets. For example, disruption of CD4+CD25+ Tregs with anti CD25 antibodies in ApoE−/− mice accelerates the development of atherosclerosis lesions and increases plaque vulnerability. Atherosclerosis is also increased in LDLR−/− mice reconstituted with bone marrow depleted of FOXP3+ Tregs using a DT-based procedure. Conversely, atherosclerosis is prevented by inducing Tregs with anti CD3 and IL-2/anti-IL2 or both monoclonal antibodies. Protection against atherosclerosis is also achieved by reducing the effector T cell to Treg ratio with anti-CD3 monoclonal antibodies or by exposure to ultraviolet B.

78We recently reported that atherosclerosis is increased in ApoE−/− mice upon inhibition of Treg recruitment in early atherosclerotic plaques by the genetic disruption of CCL1, while a similar effect is observed in LDLR−/− mice upon monoclonal antibody blockade of the CCL1-receptor CCR8, suggesting the importance of Treg recruitment in atherosclerosis development.

79Impairment of Treg function may contribute to the acceleration of atherosclerosis. Tregs from ApoE−/− mice have lower inhibitory Treg function than C57BL/6 mice, similar to the impaired Treg function observed in acute coronary syndrome patients. Similarly, CCL-1 genetic disruption reduces Treg inhibitory capacity in ApoE−/− mice fed a high-fat diet.

80The importance of Treg abundance and the effector T cell to Treg ratio in atherosclerosis is also supported by human studies. This is suggested by to the impaired Treg function observed in acute coronary syndrome patients and the low abundance of peripheral Treg in patients with acute coronary syndrome or stable angina and the higher effector T cell to Treg ratio observed in patients with coronary artery disease than in healthy individuals. Treg numbers in patients with non-ST segment elevation acute coronary syndrome are reduced by apoptosis promoted by oxLDLs.

81These data highlight the importance of the abundance and function of several Treg subsets and Treg-related cytokines in the development of atherosclerosis.

5.2. CD8 T Cells

82CD8 T cells play a prominent role in the defense against intracellular pathogens. These T cells recognize antigen via the TCR in the context of ubiquitously expressed MHC class I molecules (MHC-I; HLA-A, B, or C in humans). Upon antigen recognition, naïve CD8+ T cells are activated, proliferate, and differentiate into CD8+ CTLs. CD8 T cells play effector functions through the release of proinflammatory cytokines, such as TNF-α, which can induce apoptosis, and IFN-γ, which promotes MHC-I upregulation and further promotes the inflammatory response. CD8 T cells promote Fas receptor mediated-apoptosis of the target cell through the expression of Fas ligand and target cell lysis through the release of granzymes and perforin.

83Some studies show no effect or a protective effect of CD8 T cells in atherosclerosis, whereas others report a proatherogenic effect. A neutral or protective action is supported by unaltered atherosclerosis in ApoE−/− mice lacking antigen peptide transporter 1-(TAP1)-dependent MHC-I antigen presentation, despite the low number of CD8+ T cells in these animals. Moreover, atherosclerosis in ApoE−/− mice is also unaffected by genetic disruption of CD8a. However, increased plaque development was reported in a MHC-I deficient mouse model with reduced CD8+ T cell numbers, and the adoptive transfer of CD8+ T cells from p210 peptide of ApoB100-immunized mice slows plaque formation in recipients while expanding CD8 T cells, suggesting an antiatherogenic role for at least some CD8+ T cells. Indeed, atherosclerosis can be reduced by the cytolytic action of CD8+ T-cells on proatherogenic DCs and follicular Th cells. Moreover, the plaque microenvironment might potentiate a protective action of CD8 T cells by inducing expression of the ectonucleotidase CD39, which mediates decreased IFN-γ and TNF-α production in CD8 T cells.

84Other studies support a proatherogenic role of CD8 T cells, as suggested by the increase in CD8+ T cell number as the lesion progresses toward more advanced stages, and the increased production of IFN-γ by CD28+CD8+ T cells in major artery-draining lymph nodes in hypercholesterolemic ApoE−/− mice. Furthermore, CD8 T cell stimulation by the injection of an anti-CD137 antibody increases inflammation and plaque development, and CD8 T cell depletion in LDLR−/− mice reduces plaque formation by impeding monocyte hematopoiesis due to the decrease in systemic CD8 T-cell dependent IFN-γ. CD8+ T cells have been reported to promote atherosclerosis through the induction of apoptosis in macrophages, endothelial cells, and smooth muscle cells, leading to necrotic core formation and increased inflammation. A proatherogenic role is further suggested by the ability of CD8+ T cells to promote monocyte recruitment and augment lesion instability. Overall, these studies, thus, suggest that different CD8 T cells subsets may play opposing roles in atherosclerosis.

5.3. B-Cells

85B-cells play critical roles in innate and adaptive immunity through their capacity to produce antibodies and secrete cytokines. B cells are characterized by the expression of membrane-bound immunoglobulins, known as B cell receptor (BCRs), with exclusive epitope-binding sites. BCRs, each one unique to a single B cell clone, bind antigens and are generated by the recombination of variable (V), diversity (D), and joining (J) genes by the product of recombinase activation gene (RAG). The mature BCR and the subsequently produced antibodies are composed of duplicated copies of the recombined heavy and light immunoglobulin polypeptides. The BCR forms a complex with several other membrane proteins, including the B cell receptor CD22, receptor-type tyrosine protein phosphatase C (PTPRC, also known as B220 and CD45), and B-lymphocyte antigen CD19. BCR stimulation induces NF-κB, PI3K, and MAPK signaling, which play essential roles in B cell development, differentiation, and activation. After activation, B cells proliferate and differentiate toward a plasma cell phenotype. Differences in the Fc region define five major types of antibody: IgA, IgD, IgE, IgG, and IgM. Some of these can be divided into different subtypes.

86B cells can be subclassified as B1 and B2 cells. B1 cells derive from fetal hematopoietic stem cells and produce natural antibodies independently of Th signals, without infection or immunization. B1 cells circulate systemically and also guard mucosal surfaces, where they generate immediate protection via antigen capture and opsonization of entering bacteria. Like plasma cells, antibody-secreting B1 cells reside in the spleen and bone marrow in large numbers. In mice, B1 cells are further classified as CD5-expressing B1a cells and B1b cells. B1a cells produce spontaneous T cell-independent, long-lasting, unmutated IgM, whereas B1b cells produce IgA.

87B2 cells derive from bone-marrow precursors, which, after several maturation steps in the bone marrow and the secondary lymphoid organs, differentiate into marginal zone (MZ) B cells and follicular (FO) B cells. MZ B cells are found in the splenic marginal sinus and respond to blood-borne pathogens in a T cell-independent manner by differentiating toward antibody-secreting plasma cells. FO B cells are found in the periphery and are activated by antigens and Th cells before undergoing the germinal center reactions (class-switch recombination and somatic hypermutation) to generate switched Igs and BCRs that more precisely react with the target antigen. At the germinal center, with the help of follicular DCs and follicular helper T cells, FO B cells undergo an affinity maturation and selection procedure for antigens and then give rise to antibody-precise, antibody-generating, long-lived plasma cells or memory B cells. These plasma cells and memory B cells govern antibody-mediated immune responses. B cells also regulate T cell and macrophage differentiation and modulate inflammatory responses through the secretion of specific cytokines. Regulatory B cells (Bregs) play immunosuppressive roles through the release of IL-10, TGFβ, and IL-35.

88B cells can play protective and pathogenic roles in atherosclerosis. An atheroprotective role is supported by the increased atherosclerosis in ApoE−/− mice after splenectomy, which reduces B cells’ numbers; this effect is attenuated by the adoptive transfer of splenic B cells. Moreover, atherosclerosis is increased after the reconstitution of bone marrow-depleted LDLR−/− mice with bone marrow from B cell-deficient mice (µMT−/− mice), and this effect is also reversed by the adoptive transfer of splenic B cells. Immunization studies have confirmed the antiatherogenic role of B cell-derived antibodies, and atherosclerosis is reduced upon immunization with malondialdehyde modified LDL (MDA-LDL) or other oxLDLs.

89A proatherogenic action of B cells is revealed in ApoE−/− and LDLR−/− mice upon depletion of B2 cells with antibodies to CD20, the receptor for the B-cell survival regulator B cell activating factor receptor (BAFFR) or by genetic disruption of BAFFR

90The different B cell subclasses appear to make distinct contributions to the B cell-mediated modulation of atherosclerosis. B1a cells produce natural IgM antibodies against oxLDL and antigens derived from apoptotic cells, blocking macrophage oxLDL uptake and foam-cell generation and stimulating apoptotic cell removal from atherosclerotic plaques. Experiments in splenectomized ApoE−/− mice show that this atheroprotective effect is mediated by TLR4 and MYD88. The role of B1b cells in atherosclerosis is not fully understood; however, adoptive transfer of B1b cells to Rag1−/−/ApoE−/− mice reduces atherosclerosis.

91Atheroprotective B1 responses appear to depend on the control of the adaptive germinal center by B Cell Fcγ Receptor IIb. The studies cited above suggest a proatherogenic action of B2 cells. Bregs exert immunosuppressive functions by secreting the cytokines IL-10 and TGFβ, and IL-10 disruption promotes inflammatory cell infiltration and cytokine generation and enhances atherosclerosis in mice. An atheroprotective role of Bregs is supported by increased IL-10 production and Treg induction after the transfer of CTB-p210-pulsed Bregs or CD21hiCD23hiCD24hi Bregs. However, another study found no protective effect of Bregs. Further experiments are, therefore, needed to clarify this role.

6. Discussion

92Emerging evidence indicates that LDLs stimulate both innate and adaptive immunity in atherosclerosis. Atherosclerosis is aggravated by proinflammatory responses mediated by macrophages, Th1 cells, and B2 cells. The action of proinflammatory immune-system components is reduced by regulatory cells, such as Tregs, Bregs, M2 macrophages, and tolerogenic DCs. Regulatory-cell–mediated approaches, thus, have great potential for future therapies. However, recent findings indicate that these immunosuppressive responses can become dysfunctional due to microenvironmental factors that convert protective functions into proatherogenic responses. Several immune cells, including CD8 T cells, B1 cells, Th2 cells, Th17 cells, and some DC subsets appear to play both a protective and a proatherogenic role in the onset and progression of atherosclerosis depending on other factors, or their true function remains unresolved. Further research is, therefore, need to elucidate the specific function of these cells in human atherosclerotic disease and develop therapeutic strategies that stimulate their protective actions.

93Some studies in mice indicate that the inhibition of inflammatory processes in advanced atherosclerotic lesions allows atheroprotective immune responses to promote plaque regression. In humans, the CANTOS trial of the anti-IL-1β blocking antibody canakinumab in patients with a history of myocardial infarction and elevated serum hsCRP (high-sensitivity C-reactive protein) demonstrates that inflammation is a direct cause of the onset and development of atherosclerosis. This clinical trial also highlights the importance of inflammation as a target for future treatments to reduce atherosclerosis. However, low dose methotrexate (MTX) treatment—included in the CIRT study and aimed to reduce inflammation and cardiovascular risk in patients with previous myocardial infarction or multivessel coronary disease who have indirect evidence of inflammatory risk, by additionally having either type 2 diabetes or the metabolic syndrome—fails to reduce cardiovascular events. Contrasting with anti-IL-1β blocking antibody canakinumab treatment, MTX did not result in lower IL-1β, IL-6, or hsCRP levels than placebo. This may due to the fact that MTX function and molecular targets are different from the canakinumab, affecting less relevant pathogenic pathways in atherosclerosis. Moreover, CANTOS and CIRT trials also differ in the population of study. Nevertheless, it is important to weigh the potential dangers of this type of anti-inflammatory therapy; risks include aggravating or potentiating undesired effects, such as infection and cancer. In the CANTOS trial, canakinumab increased the incidence of fatal infection and sepsis and in the CIRT study, a slight increase in skin tumors was observed over time in the MTX treated population. Further studies are needed to determine the importance for the essential inflammatory responses of many potential therapeutic targets in the prevention and treatment of atherosclerosis.

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Benjamin E.J., Blaha M.J., Chiuve S.E., Cushman M., Das S.R., Deo R., de Ferranti S.D., Floyd J., Fornage M., Gillespie C., et al. Heart Disease and Stroke Statistics-2017 Update: A Report from the American Heart Association. Circulation. 2017;135:e146-e603.
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20.
Ross R. Atherosclerosis–An Inflammatory Disease. N. Engl. J. Med. 1999;340:115-126.
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21.
Hansson G.K. Inflammation, Atherosclerosis, and Coronary Artery Disease. N. Engl. J. Med. 2005;352:1685-1695.
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23.
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24.
Tanaka S., Matsumoto T., Matsubara Y., Harada Y., Kyuragi R., Koga J.I., Egashira K., Nakashima Y., Yonemitsu Y., Maehara Y. BubR1 Insufficiency Results in Decreased Macrophage Proliferation and Attenuated Atherogenesis in Apolipoprotein E-Deficient Mice. J. Am. Heart Assoc. 2016;5:e004081.
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Chatzizisis Y.S., Coskun A.U., Jonas M., Edelman E.R., Feldman C.L., Stone P.H. Role of Endothelial Shear Stress in the Natural History of Coronary Atherosclerosis and Vascular Remodeling: Molecular, Cellular and Vascular Behavior. J. Am. Coll. Cardiol. 2007;49:2379-2393.
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Dai G., Kaazempur-Mofrad M.R., Natarajan S., Zhang Y., Vaughn S., Blackman B.R., Kamm R.D., Garcia-Cardena G., Gimbrone M.A. Distinct Endothelial Phenotypes Evoked by Arterial Waveforms Derived from Atherosclerosis-Susceptible and -Resistant Regions of Human Vasculature. Proc. Natl. Acad. Sci. USA. 2004;101:14871-14876.
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Lipton B.A., Parthasarathy S., Ord V.A., Clinton S.K., Libby P., Rosenfeld M.E. Components of the Protein Fraction of Oxidized Low Density Lipoprotein Stimulate Interleukin-1 Alpha Production by Rabbit Arterial Macrophage-Derived foam Cells. J. Lipid. Res. 1995;36:2232-2242.
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29.
Kranzhofer R., Schmidt J., Pfeiffer C.A., Hagl S., Libby P., Kubler W. Angiotensin Induces Inflammatory Activation of Human Vascular Smooth Muscle Cells. Arterioscler. Thromb. Vasc. Biol. 1999;19:1623-1629.
Not in our library10.1161/01.atv.19.7.1623
30.
Libby P., Ordovas J.M., Auger K.R., Robbins A.H., Birinyi L.K., Dinarello C.A. Endotoxin and Tumor Necrosis Factor Induce Interleukin-1 Gene Expression in Adult Human Vascular Endothelial Cells. Am. J. Pathol. 1986;124:179-185.
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31.
Libby P., Ridker P.M., Maseri A. Inflammation and Atherosclerosis. Circulation. 2002;105:1135-1143.
Not in our library10.1161/hc0902.104353
32.
Mannarino E., Pirro M. Endothelial Injury and Repair: A Novel Theory for Atherosclerosis. Angiology. 2008;59:69S-72S.
Not in our library10.1177/0003319708320761
33.
Clinton S.K., Underwood R., Hayes L., Sherman M.L., Kufe D.W., Libby P. Macrophage Colony-Stimulating Factor Gene Expression in Vascular Cells and in Experimental and Human Atherosclerosis. Am. J. Pathol. 1992;140:301-316.
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34.
Galkina E., Ley K. Vascular Adhesion Molecules in Atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 2007;27:2292-2301.
Not in our library10.1161/atvbaha.107.149179
35.
Libby P., Ridker P.M., Hansson G.K. Leducq Transatlantic Network on Atherothrombosis. Inflammation in Atherosclerosis: From Pathophysiology to Practice. J. Am. Coll. Cardiol. 2009;54:2129-2138.
Not in our library10.1016/j.jacc.2009.09.009
36.
Macrophages and Their Role in Atherosclerosis: Pathophysiology and Transcriptome Analysis · 2016
No notice
37.
Allahverdian S., Pannu P.S., Francis G.A. Contribution of Monocyte-Derived Macrophages and Smooth Muscle Cells to Arterial Foam Cell Formation. Cardiovasc. Res. 2012;95:165-172.
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38.
Binder C.J., Papac-Milicevic N., Witztum J.L. Innate Sensing of Oxidation-Specific Epitopes in Health and Disease. Nat. Rev. Immunol. 2016;16:485-497.
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39.
Song M., Xu S., Zhong A., Zhang J. Crosstalk between Macrophage and T Cell in Atherosclerosis: Potential Therapeutic Targets for Cardiovascular Diseases. Clin. Immunol. 2019;202:11-17.
Not in our library10.1016/j.clim.2019.03.001
40.
Worbs T., Hammerschmidt S.I., Forster R. Dendritic Cell Migration in Health and Disease. Nat. Rev. Immunol. 2017;17:30-48.
Not in our library10.1038/nri.2016.116
41.
Gil-Pulido J., Zernecke A. Antigen-Presenting Dendritic Cells in Atherosclerosis. Eur. J. Pharmacol. 2017;816:25-31.
Not in our library10.1016/j.ejphar.2017.08.016
42.
Sage A.P., Tsiantoulas D., Binder C.J., Mallat Z. The Role of B Cells in Atherosclerosis. Nat. Rev. Cardiol. 2019;16:180-196.
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43.
Hansson G.K., Libby P., Schonbeck U., Yan Z.Q. Innate and Adaptive Immunity in the Pathogenesis of Atherosclerosis. Circ. Res. 2002;91:281-291.
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45.
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46.
Jonasson L., Holm J., Skalli O., Bondjers G., Hansson G.K. Regional Accumulations of T Cells, Macrophages and Smooth Muscle Cells in the Human Atherosclerotic Plaque. Arteriosclerosis. 1986;6:131-138.
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47.
Kovanen P.T., Kaartinen M., Paavonen T. Infiltrates of Activated Mast Cells at the Site of Coronary Atheromatous Erosion or Rupture in Myocardial Infarction. Circulation. 1995;92:1084-1088.
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48.
Obikane H., Abiko Y., Ueno H., Kusumi Y., Esumi M., Mitsumata M. Effect of Endothelial Cell Proliferation on Atherogenesis: A Role of p21(Sdi/Cip/Waf1) in Monocyte Adhesion to Endothelial Cells. Atherosclerosis. 2010;212:116-122.
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49.
Libby P., Okamoto Y., Rocha V.Z., Folco E. Inflammation in Atherosclerosis: Transition from Theory to Practice. Circ. J. 2010;74:213-220.
Not in our library10.1253/circj.cj-09-0706
50.
Verma S., Wang C.H., Li S.H., Dumont A.S., Fedak P.W., Badiwala M.V., Dhillon B., Weisel R.D., Li R.K., Mickle D.A., et al. A Self-Fulfilling Prophecy: C-Reactive Protein Attenuates Nitric Oxide Production and Inhibits Angiogenesis. Circulation. 2002;106:913-919.
Not in our library10.1161/01.cir.0000029802.88087.5e
51.
Quillard T., Tesmenitsky Y., Croce K., Travers R., Shvartz E., Koskinas K.C., Sukhova G.K., Aikawa E., Aikawa M., Libby P. Selective Inhibition of Matrix Metalloproteinase-13 Increases Collagen Content of Established Mouse Atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 2011;31:2464-2472.
Not in our library10.1161/atvbaha.111.231563
52.
Schneider F., Sukhova G.K., Aikawa M., Canner J., Gerdes N., Tang S.M., Shi G.P., Apte S.S., Libby P. Matrix-Metalloproteinase-14 Deficiency in Bone-Marrow-Derived Cells Promotes Collagen Accumulation in Mouse Atherosclerotic Plaques. Circulation. 2008;117:931-939.
Not in our library10.1161/circulationaha.107.707448
53.
Geng Y.J., Wu Q., Muszynski M., Hansson G.K., Libby P. Apoptosis of Vascular Smooth Muscle Cells Induced by In Vitro Stimulation with Interferon-Gamma, Tumor Necrosis Factor-Alpha and Interleukin-1 Beta. Arterioscler. Thromb. Vasc. Biol. 1996;16:19-27.
Not in our library10.1161/01.atv.16.1.19
54.
Houtkamp M.A., de Boer O.J., van der Loos C.M., van der Wal A.C., Becker A.E. Adventitial Infiltrates Associated with Advanced Atherosclerotic Plaques: Structural Organization Suggests Generation of Local Humoral Immune Responses. J. Pathol. 2001;193:263-269.
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55.
Moos M.P., John N., Grabner R., Nossmann S., Gunther B., Vollandt R., Funk C.D., Kaiser B., Habenicht A.J. The Lamina Adventitia is the Major Site of Immune Cell Accumulation in Standard Chow-fed Apolipoprotein E-Deficient mice. Arterioscler. Thromb. Vasc. Biol. 2005;25:2386-2391.
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56.
Taylor P.R., Gordon S. Monocyte Heterogeneity and Innate Immunity. Immunity. 2003;19:2-4.
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57.
van Furth R., Cohn Z.A. The Origin and Kinetics of Mononuclear Phagocytes. J. Exp. Med. 1968;128:415-435.
Not in our library10.1084/jem.128.3.415
58.
From Monocytes to M1/M2 Macrophages: Phenotypical vs. Functional Differentiation · 2014
No notice
59.
Camici P.G., Rimoldi O.E., Gaemperli O., Libby P. Non-Invasive Anatomic and Functional Imaging of Vascular Inflammation and Unstable Plaque. Eur. Heart J. 2012;33:1309-1317.
Not in our library10.1093/eurheartj/ehs067
60.
Combadiere C., Potteaux S., Rodero M., Simon T., Pezard A., Esposito B., Merval R., Proudfoot A., Tedgui A., Mallat Z. Combined Inhibition of CCL2, CX3CR1 and CCR5 Abrogates Ly6C(hi) and Ly6C(lo) Monocytosis and Almost Abolishes Atherosclerosis in Hypercholesterolemic Mice. Circulation. 2008;117:1649-1657.
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61.
Takeya M., Yoshimura T., Leonard E.J., Takahashi K. Detection of Monocyte Chemoattractant Protein-1 in Human Atherosclerotic Lesions by an Anti-Monocyte Chemoattractant Protein-1 Monoclonal Antibody. Hum. Pathol. 1993;24:534-539.
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62.
Yla-Herttuala S., Lipton B.A., Rosenfeld M.E., Sarkioja T., Yoshimura T., Leonard E.J., Witztum J.L., Steinberg D. Expression of Monocyte Chemoattractant Protein 1 in Macrophage-Rich Areas of Human and Rabbit Atherosclerotic Lesions. Proc. Natl. Acad. Sci. USA. 1991;88:5252-5256.
Not in our library10.1073/pnas.88.12.5252
63.
Lin J., Kakkar V., Lu X. Impact of MCP-1 in Atherosclerosis. Curr. Pharm. Des. 2014;20:4580-4588.
Not in our library10.2174/1381612820666140522115801
64.
Boisvert W.A., Rose D.M., Johnson K.A., Fuentes M.E., Lira S.A., Curtiss L.K., Terkeltaub R.A. Up-Regulated Expression of the CXCR2 Ligand KC/GRO-Alpha in Atherosclerotic Lesions Plays a Central Role in Macrophage Accumulation and Lesion Progression. Am. J. Pathol. 2006;168:1385-1395.
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65.
Zernecke A., Liehn E.A., Gao J.L., Kuziel W.A., Murphy P.M., Weber C. Deficiency in CCR5 but not CCR1 Protects Against Neointima Formation in Atherosclerosis-Prone Mice: Involvement of IL-10. Blood. 2006;107:4240-4243.
Not in our library10.1182/blood-2005-09-3922
66.
Koenen R.R., von Hundelshausen P., Nesmelova I.V., Zernecke A., Liehn E.A., Sarabi A., Kramp B.K., Piccinini A.M., Paludan S.R., Kowalska M.A., et al. Disrupting Functional Interactions between Platelet Chemokines Inhibits Atherosclerosis in Hyperlipidemic Mice. Nat. Med. 2009;15:97-103.
Not in our library10.1038/nm.1898
67.
The Role of Monocytes and Macrophages in Human Atherosclerosis, Plaque Neoangiogenesis, and Atherothrombosis · 2019
Not checked
68.
Ziegler-Heitbrock L. The CD14+ CD16+ Blood Monocytes: Their Role in Infection and Inflammation. J. Leukoc. Biol. 2007;81:584-592.
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Ziegler-Heitbrock L., Ancuta P., Crowe S., Dalod M., Grau V., Hart D.N., Leenen P.J., Liu Y.J., MacPherson G., Randolph G.J., et al. Nomenclature of Monocytes and Dendritic Cells in Blood. Blood. 2010;116:e74-e80.
Not in our library10.1182/blood-2010-02-258558
70.
Rogacev K.S., Cremers B., Zawada A.M., Seiler S., Binder N., Ege P., Grosse-Dunker G., Heisel I., Hornof F., Jeken J., et al. CD14++CD16+ Monocytes Independently Predict Cardiovascular Events: A Cohort Study of 951 Patients Referred for Elective Coronary Angiography. J. Am. Coll. Cardiol. 2012;60:1512-1520.
Not in our library10.1016/j.jacc.2012.07.019
71.
Sala F., Cutuli L., Grigore L., Pirillo A., Chiesa G., Catapano A.L., Norata G.D. Prevalence of Classical CD14++/CD16- but not of Intermediate CD14++/CD16+ Monocytes in Hypoalphalipoproteinemia. Int. J. Cardiol. 2013;168:2886-2889.
Not in our library10.1016/j.ijcard.2013.03.103
72.
Belge K.U., Dayyani F., Horelt A., Siedlar M., Frankenberger M., Frankenberger B., Espevik T., Ziegler-Heitbrock L. The Proinflammatory CD14+CD16+DR++ Monocytes are a Major Source of TNF. J. Immunol. 2002;168:3536-3542.
Not in our library10.4049/jimmunol.168.7.3536
73.
Human Dendritic Cell Functional Specialization in Steady-State and Inflammation · 2014
No notice
74.
Liu K., Victora G.D., Schwickert T.A., Guermonprez P., Meredith M.M., Yao K., Chu F.F., Randolph G.J., Rudensky A.Y., Nussenzweig M. In Vivo Analysis of Dendritic Cell Development and Homeostasis. Science. 2009;324:392-397.
Not in our library10.1126/science.1170540
75.
Zhao C., Zhang H., Wong W.C., Sem X., Han H., Ong S.M., Tan Y.C., Yeap W.H., Gan C.S., Ng K.Q., et al. Identification of Novel Functional Differences in Monocyte Subsets Using Proteomic and Transcriptomic Methods. J. Proteome Res. 2009;8:4028-4038.
Not in our library10.1021/pr900364p
76.
Evans H.G., Gullick N.J., Kelly S., Pitzalis C., Lord G.M., Kirkham B.W., Taams L.S. In Vivo Activated Monocytes from the Site of Inflammation in Humans Specifically Promote Th17 Responses. Proc. Natl. Acad. Sci. USA. 2009;106:6232-6237.
Not in our library10.1073/pnas.0808144106
77.
Serbina N.V., Jia T., Hohl T.M., Pamer E.G. Monocyte-Mediated Defense against Microbial Pathogens. Annu. Rev. Immunol. 2008;26:421-452.
Not in our library10.1146/annurev.immunol.26.021607.090326
78.
Avraham-Davidi I., Yona S., Grunewald M., Landsman L., Cochain C., Silvestre J.S., Mizrahi H., Faroja M., Strauss-Ayali D., Mack M., et al. On-Site Education of VEGF-Recruited Monocytes Improves Their Performance as Angiogenic and Arteriogenic Accessory Cells. J. Exp. Med. 2013;210:2611-2625.
Not in our library10.1084/jem.20120690
79.
Swirski F.K., Libby P., Aikawa E., Alcaide P., Luscinskas F.W., Weissleder R., Pittet M.J. Ly-6Chi Monocytes Dominate Hypercholesterolemia-Associated Monocytosis and Give Rise to Macrophages in Atheromata. J. Clin. Investig. 2007;117:195-205.
Not in our library10.1172/jci29950
80.
Justo-Junior A.S., Villarejos L.M., Lima X.T.V., Nadruz W., Sposito A.C., Mamoni R.L., Abdalla R., Fernandes J.L., Oliveira R.T.D., Blotta M. Monocytes of Patients with Unstable Angina Express High Levels of Chemokine and Pattern-Recognition Receptors. Cytokine. 2019;113:61-67.
Not in our library10.1016/j.cyto.2018.06.008
81.
Ozaki Y., Imanishi T., Hosokawa S., Nishiguchi T., Taruya A., Tanimoto T., Kuroi A., Yamano T., Matsuo Y., Ino Y., et al. Association of Toll-Like Receptor 4 on Human Monocyte Subsets and Vulnerability Characteristics of Coronary Plaque as Assessed by 64-Slice Multidetector Computed Tomography. Circ. J. 2017;81:837-845.
Not in our library10.1253/circj.cj-16-0688
82.
Cybulsky M.I., Iiyama K., Li H., Zhu S., Chen M., Iiyama M., Davis V., Gutierrez-Ramos J.C., Connelly P.W., Milstone D.S. A Major Role for VCAM-1, but not ICAM-1, in Early Atherosclerosis. J. Clin. Investig. 2001;107:1255-1262.
Not in our library10.1172/jci11871
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Sundell C.L., Somers P.K., Meng C.Q., Hoong L.K., Suen K.L., Hill R.R., Landers L.K., Chapman A., Butteiger D., Jones M., et al. AGI-1067: A Multifunctional Phenolic Antioxidant, Lipid Modulator, Anti-Inflammatory and Antiatherosclerotic Agent. J. Pharmacol. Exp. Ther. 2003;305:1116-1123.
Not in our library10.1124/jpet.102.048132
84.
Qiao J.H., Tripathi J., Mishra N.K., Cai Y., Tripathi S., Wang X.P., Imes S., Fishbein M.C., Clinton S.K., Libby P., et al. Role of Macrophage Colony-Stimulating Factor in Atherosclerosis: Studies of Osteopetrotic Mice. Am. J. Pathol. 1997;150:1687-1699.
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85.
Nicola N.A., Metcalf D. Specificity of Action of Colony-Stimulating Factors in the Differentiation of Granulocytes and Macrophages. Ciba Found. Symp. 1986;118:7-28.
Not in our library10.1002/9780470720998.ch2
86.
Woollard K.J., Geissmann F. Monocytes in Atherosclerosis: Subsets and Functions. Nat. Rev. Cardiol. 2010;7:77-86.
Not in our library10.1038/nrcardio.2009.228
87.
Zhou X., Hansson G.K. Detection of B Cells and Proinflammatory Cytokines in Atherosclerotic Plaques of Hypercholesterolaemic Apolipoprotein E Knockout Mice. Scand. J. Immunol. 1999;50:25-30.
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88.
Randolph G.J. Mechanisms that Regulate Macrophage Burden in Atherosclerosis. Circ. Res. 2014;114:1757-1771.
Not in our library10.1161/circresaha.114.301174
89.
Moore K.J., Sheedy F.J., Fisher E.A. Macrophages in Atherosclerosis: A Dynamic Balance. Nat. Rev. Immunol. 2013;13:709-721.
Not in our library10.1038/nri3520
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Tacke F., Alvarez D., Kaplan T.J., Jakubzick C., Spanbroek R., Llodra J., Garin A., Liu J., Mack M., van Rooijen N., et al. Monocyte Subsets Differentially Employ CCR2, CCR5, and CX3CR1 to Accumulate within Atherosclerotic Plaques. J. Clin. Investig. 2007;117:185-194.
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91.
Robbins C.S., Hilgendorf I., Weber G.F., Theurl I., Iwamoto Y., Figueiredo J.L., Gorbatov R., Sukhova G.K., Gerhardt L.M., Smyth D., et al. Local Proliferation Dominates Lesional Macrophage Accumulation in Atherosclerosis. Nat. Med. 2013;19:1166-1172.
Not in our library10.1038/nm.3258
92.
Li Q., Park K., Xia Y., Matsumoto M., Qi W., Fu J., Yokomizo H., Khamaisi M., Wang X., Rask-Madsen C., et al. Regulation of Macrophage Apoptosis and Atherosclerosis by Lipid-Induced PKCdelta Isoform Activation. Circ. Res. 2017;121:1153-1167.
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93.
Shashkin P., Dragulev B., Ley K. Macrophage Differentiation to Foam Cells. Curr. Pharm. Des. 2005;11:3061-3072.
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94.
Seimon T., Tabas I. Mechanisms and Consequences of Macrophage Apoptosis in Atherosclerosis. J. Lipid. Res. 2009;50(Suppl.):S382-S387.
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95.
Tajbakhsh A., Rezaee M., Kovanen P.T., Sahebkar A. Efferocytosis in Atherosclerotic Lesions: Malfunctioning Regulatory Pathways and Control Mechanisms. Pharmacol. Ther. 2018;188:12-25.
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96.
Thorp E., Subramanian M., Tabas I. The Role of Macrophages and Dendritic Cells in the Clearance of Apoptotic Cells in Advanced Atherosclerosis. Eur. J. Immunol. 2011;41:2515-2518.
Not in our library10.1002/eji.201141719
97.
Thorp E., Tabas I. Mechanisms and Consequences of Efferocytosis in Advanced Atherosclerosis. J. Leukoc. Biol. 2009;86:1089-1095.
Not in our library10.1189/jlb.0209115
98.
Murray P.J., Allen J.E., Biswas S.K., Fisher E.A., Gilroy D.W., Goerdt S., Gordon S., Hamilton J.A., Ivashkiv L.B., Lawrence T., et al. Macrophage Activation and Polarization: Nomenclature and Experimental Guidelines. Immunity. 2014;41:14-20.
Not in our library10.1016/j.immuni.2014.06.008
99.
Martinez F.O., Sica A., Mantovani A., Locati M. Macrophage Activation and Polarization. Front. Biosci. 2008;13:453-461.
Not in our library10.2741/2692
100.
Porcheray F., Viaud S., Rimaniol A.C., Leone C., Samah B., Dereuddre-Bosquet N., Dormont D., Gras G. Macrophage Activation Switching: An Asset for the Resolution of Inflammation. Clin. Exp. Immunol. 2005;142:481-489.
Not in our library10.1111/j.1365-2249.2005.02934.x
101.
Lee S., Huen S., Nishio H., Nishio S., Lee H.K., Choi B.S., Ruhrberg C., Cantley L.G. Distinct Macrophage Phenotypes Contribute to Kidney Injury and Repair. J. Am. Soc. Nephrol. 2011;22:317-326.
Not in our library10.1681/asn.2009060615
102.
Feig J.E., Rong J.X., Shamir R., Sanson M., Vengrenyuk Y., Liu J., Rayner K., Moore K., Garabedian M., Fisher E.A. HDL Promotes Rapid Atherosclerosis Regression in Mice and Alters Inflammatory Properties of Plaque Monocyte-Derived Cells. Proc. Natl. Acad. Sci. USA. 2011;108:7166-7171.
Not in our library10.1073/pnas.1016086108
103.
Lavin Y., Winter D., Blecher-Gonen R., David E., Keren-Shaul H., Merad M., Jung S., Amit I. Tissue-Resident Macrophage Enhancer Landscapes are Shaped by the Local Microenvironment. Cell. 2014;159:1312-1326.
Not in our library10.1016/j.cell.2014.11.018
104.
Van den Bossche J., O’Neill L.A., Menon D. Macrophage Immunometabolism: Where Are We (Going)? Trends Immunol. 2017;38:395-406.
Not in our library10.1016/j.it.2017.03.001
105.
Joseph P., Tawakol A. Imaging Atherosclerosis with Positron Emission Tomography. Eur. Heart J. 2016;37:2974-2980.
Not in our library10.1093/eurheartj/ehw147
106.
Wang Z., Klipfell E., Bennett B.J., Koeth R., Levison B.S., Dugar B., Feldstein A.E., Britt E.B., Fu X., Chung Y.M., et al. Gut Flora Metabolism of Phosphatidylcholine Promotes Cardiovascular Disease. Nature. 2011;472:57-63.
Not in our library10.1038/nature09922
107.
Phan A.T., Goldrath A.W., Glass C.K. Metabolic and Epigenetic Coordination of T Cell and Macrophage Immunity. Immunity. 2017;46:714-729.
Not in our library10.1016/j.immuni.2017.04.016
108.
Martinez F.O., Gordon S., Locati M., Mantovani A. Transcriptional Profiling of the Human Monocyte-to-Macrophage Differentiation and Polarization: New Molecules and Patterns of Gene Expression. J. Immunol. 2006;177:7303-7311.
Not in our library10.4049/jimmunol.177.10.7303
109.
Shapouri-Moghaddam A., Mohammadian S., Vazini H., Taghadosi M., Esmaeili S.A., Mardani F., Seifi B., Mohammadi A., Afshari J.T., Sahebkar A. Macrophage Plasticity, Polarization and Function in Health and Disease. J. Cell. Physiol. 2018;233:6425-6440.
Not in our library10.1002/jcp.26429
110.
Shortman K., Liu Y.J. Mouse and Human Dendritic Cell Subtypes. Nat. Rev. Immunol. 2002;2:151-161.
Not in our library10.1038/nri746
111.
Waldo S.W., Li Y., Buono C., Zhao B., Billings E.M., Chang J., Kruth H.S. Heterogeneity of Human Macrophages in Culture and in Atherosclerotic Plaques. Am. J. Pathol. 2008;172:1112-1126.
Not in our library10.2353/ajpath.2008.070513
112.
Hoeve M.A., Savage N.D., de Boer T., Langenberg D.M., de Waal Malefyt R., Ottenhoff T.H., Verreck F.A. Divergent Effects of IL-12 and IL-23 on the Production of IL-17 by Human T Cells. Eur. J. Immunol. 2006;36:661-670.
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113.
Brocheriou I., Maouche S., Durand H., Braunersreuther V., Le Naour G., Gratchev A., Koskas F., Mach F., Kzhyshkowska J., Ninio E. Antagonistic Regulation of Macrophage Phenotype by M-CSF and GM-CSF: Implication in Atherosclerosis. Atherosclerosis. 2011;214:316-324.
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114.
Burgess A.W., Metcalf D. The Nature and Action of Granulocyte-Macrophage Colony Stimulating Factors. Blood. 1980;56:947-958.
Not in our library10.1182/blood.v56.6.947.947
115.
Gasson J.C. Molecular Physiology of Granulocyte-Macrophage Colony-Stimulating Factor. Blood. 1991;77:1131-1145.
Not in our library10.1182/blood.v77.6.1131.1131
116.
Plenz G., Koenig C., Severs N.J., Robenek H. Smooth Muscle Cells Express Granulocyte-Macrophage Colony-Stimulating Factor in the Undiseased and Atherosclerotic Human Coronary Artery. Arterioscler. Thromb. Vasc. Biol. 1997;17:2489-2499.
Not in our library10.1161/01.atv.17.11.2489
117.
Lacave-Lapalun J.V., Benderitter M., Linard C. Flagellin or Lipopolysaccharide Treatment Modified Macrophage Populations after Colorectal Radiation of Rats. J. Pharmacol. Exp. Ther. 2013;346:75-85.
Not in our library10.1124/jpet.113.204040
118.
Verreck F.A., de Boer T., Langenberg D.M., Hoeve M.A., Kramer M., Vaisberg E., Kastelein R., Kolk A., de Waal-Malefyt R., Ottenhoff T.H. Human IL-23-Producing Type 1 Macrophages Promote but IL-10-Producing Type 2 Macrophages Subvert Immunity to (myco)Bacteria. Proc. Natl. Acad. Sci. USA. 2004;101:4560-4565.
Not in our library10.1073/pnas.0400983101
119.
Mosser D.M. The Many Faces of Macrophage Activation. J. Leukoc. Biol. 2003;73:209-212.
Not in our library10.1189/jlb.0602325
120.
Chistiakov D.A., Bobryshev Y.V., Nikiforov N.G., Elizova N.V., Sobenin I.A., Orekhov A.N. Macrophage Phenotypic Plasticity in Atherosclerosis: The Associated Features and the Peculiarities of the Expression of Inflammatory Genes. Int. J. Cardiol. 2015;184:436-445.
Not in our library10.1016/j.ijcard.2015.03.055
121.
Zizzo G., Hilliard B.A., Monestier M., Cohen P.L. Efficient Clearance of Early Apoptotic Cells by Human Macrophages Requires M2c Polarization and MerTK Induction. J. Immunol. 2012;189:3508-3520.
Not in our library10.4049/jimmunol.1200662
122.
Chistiakov D.A., Bobryshev Y.V., Orekhov A.N. Changes in Transcriptome of Macrophages in Atherosclerosis. J. Cell. Mol. Med. 2015;19:1163-1173.
Not in our library10.1111/jcmm.12591
123.
Mantovani A., Sica A., Sozzani S., Allavena P., Vecchi A., Locati M. The Chemokine System in Diverse Forms of Macrophage Activation and Polarization. Trends Immunol. 2004;25:677-686.
Not in our library10.1016/j.it.2004.09.015
124.
Ferrante C.J., Pinhal-Enfield G., Elson G., Cronstein B.N., Hasko G., Outram S., Leibovich S.J. The Adenosine-Dependent Angiogenic Switch of Macrophages to an M2-like Phenotype is Independent of Interleukin-4 Receptor Alpha (IL-4Ralpha) Signaling. Inflammation. 2013;36:921-931.
Not in our library10.1007/s10753-013-9621-3
125.
Anderson C.F., Gerber J.S., Mosser D.M. Modulating Macrophage Function with IgG Immune Complexes. J. Endotoxin Res. 2002;8:477-481.
Not in our library10.1177/09680519020080060501
126.
Kadl A., Sharma P.R., Chen W., Agrawal R., Meher A.K., Rudraiah S., Grubbs N., Sharma R., Leitinger N. Oxidized Phospholipid-Induced Inflammation is Mediated by Toll-Like Receptor 2. Free Radic. Biol. Med. 2011;51:1903-1909.
Not in our library10.1016/j.freeradbiomed.2011.08.026
127.
Kadl A., Meher A.K., Sharma P.R., Lee M.Y., Doran A.C., Johnstone S.R., Elliott M.R., Gruber F., Han J., Chen W., et al. Identification of a Novel Macrophage Phenotype that Develops in Response to Atherogenic Phospholipids via Nrf2. Circ. Res. 2010;107:737-746.
Not in our library10.1161/circresaha.109.215715
128.
Marques L., Negre-Salvayre A., Costa L., Canonne-Hergaux F. Iron Gene Expression Profile in Atherogenic Mox Macrophages. Biochim. Biophys. Acta. 2016;1862:1137-1146.
Not in our library10.1016/j.bbadis.2016.03.004
129.
Liberale L., Dallegri F., Montecucco F., Carbone F. Pathophysiological Relevance of Macrophage Subsets in Atherogenesis. Thromb. Haemost. 2017;117:7-18.
Not in our library10.1160/th16-08-0593
130.
Gill N., Leng Y., Romero R., Xu Y., Panaitescu B., Miller D., Arif A., Mumuni S., Qureshi F., Hsu C.D., et al. The Immunophenotype of Decidual Macrophages in Acute Atherosis. Am. J. Reprod. Immunol. 2019;81:e13098.
Not in our library10.1111/aji.13098
131.
Kockx M.M., Cromheeke K.M., Knaapen M.W., Bosmans J.M., De Meyer G.R., Herman A.G., Bult H. Phagocytosis and Macrophage Activation Associated with Hemorrhagic Microvessels in Human Atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 2003;23:440-446.
Not in our library10.1161/01.atv.0000057807.28754.7f
132.
Ganz T. Macrophages and Systemic Iron Homeostasis. J. Innate Immun. 2012;4:446-453.
Not in our library10.1159/000336423
133.
Boyle J.J., Johns M., Kampfer T., Nguyen A.T., Game L., Schaer D.J., Mason J.C., Haskard D.O. Activating Transcription Factor 1 Directs Mhem Atheroprotective Macrophages through Coordinated Iron Handling and Foam Cell Protection. Circ. Res. 2012;110:20-33.
Not in our library10.1161/circresaha.111.247577
134.
The Role of Iron Metabolism as a Mediator of Macrophage Inflammation and Lipid Handling in Atherosclerosis · 2014
Not checked
135.
Nielsen M.J., Moller H.J., Moestrup S.K. Hemoglobin and Heme Scavenger Receptors. Antioxid. Redox Signal. 2010;12:261-273.
Not in our library10.1089/ars.2009.2792
136.
Wan X., Huo Y., Johns M., Piper E., Mason J.C., Carling D., Haskard D.O., Boyle J.J. 5’-AMP-Activated Protein Kinase-Activating Transcription Factor 1 Cascade Modulates Human Monocyte-Derived Macrophages to Atheroprotective Functions in Response to Heme or Metformin. Arterioscler. Thromb. Vasc. Biol. 2013;33:2470-2480.
Not in our library10.1161/atvbaha.113.300986
137.
Boyle J.J. Heme and Haemoglobin Direct Macrophage Mhem Phenotype and Counter Foam Cell Formation in Areas of Intraplaque Haemorrhage. Curr. Opin. Lipidol. 2012;23:453-461.
Not in our library10.1097/mol.0b013e328356b145
138.
Boyle J.J., Harrington H.A., Piper E., Elderfield K., Stark J., Landis R.C., Haskard D.O. Coronary Intraplaque Hemorrhage Evokes a Novel Atheroprotective Macrophage Phenotype. Am. J. Pathol. 2009;174:1097-1108.
Not in our library10.2353/ajpath.2009.080431
139.
Pitsilos S., Hunt J., Mohler E.R., Prabhakar A.M., Poncz M., Dawicki J., Khalapyan T.Z., Wolfe M.L., Fairman R., Mitchell M., et al. Platelet Factor 4 Localization in Carotid Atherosclerotic Plaques: Correlation with Clinical Parameters. Thromb. Haemost. 2003;90:1112-1120.
Not in our library10.1160/th03-02-0069
140.
Gleissner C.A., Ley K. CXCL4 in Atherosclerosis: Possible Roles in Monocyte Arrest and Macrophage Foam Cell Formation. Thromb. Haemost. 2007;98:917-918.
Not in our library10.1160/th07-09-0567
141.
Chinetti-Gbaguidi G., Colin S., Staels B. Macrophage Subsets in Atherosclerosis. Nat. Rev. Cardiol. 2015;12:10-17.
Not in our library10.1038/nrcardio.2014.173
142.
Gleissner C.A., Shaked I., Little K.M., Ley K. CXC Chemokine Ligand 4 Induces a Unique Transcriptome in Monocyte-Derived Macrophages. J. Immunol. 2010;184:4810-4818.
Not in our library10.4049/jimmunol.0901368
143.
Erbel C., Okuyucu D., Akhavanpoor M., Zhao L., Wangler S., Hakimi M., Doesch A., Dengler T.J., Katus H.A., Gleissner C.A. A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology. J. Vis. Exp. 2014;87.
Not in our library10.3791/50542
144.
Moore K.J., Tabas I. Macrophages in the Pathogenesis of Atherosclerosis. Cell. 2011;145:341-355.
Not in our library10.1016/j.cell.2011.04.005
145.
De Paoli F., Staels B., Chinetti-Gbaguidi G. Macrophage Phenotypes and Their Modulation in Atherosclerosis. Circ. J. 2014;78:1775-1781.
Not in our library10.1253/circj.cj-14-0621
146.
Cochain C., Zernecke A. Macrophages and Immune Cells in Atherosclerosis: Recent Advances and Novel Concepts. Basic Res. Cardiol. 2015;110:34.
Not in our library10.1007/s00395-015-0491-8
147.
Bouhlel M.A., Derudas B., Rigamonti E., Dievart R., Brozek J., Haulon S., Zawadzki C., Jude B., Torpier G., Marx N., et al. PPARgamma Activation Primes Human Monocytes into Alternative M2 Macrophages with Anti-Inflammatory Properties. Cell Metab. 2007;6:137-143.
Not in our library10.1016/j.cmet.2007.06.010
148.
Gleissner C.A., Shaked I., Erbel C., Bockler D., Katus H.A., Ley K. CXCL4 Downregulates the Atheroprotective Hemoglobin Receptor CD163 in Human Macrophages. Circ. Res. 2010;106:203-211.
Not in our library10.1161/circresaha.109.199505
149.
Stoger J.L., Gijbels M.J., van der Velden S., Manca M., van der Loos C.M., Biessen E.A., Daemen M.J., Lutgens E., de Winther M.P. Distribution of Macrophage Polarization Markers in Human Atherosclerosis. Atherosclerosis. 2012;225:461-468.
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150.
Chinetti-Gbaguidi G., Baron M., Bouhlel M.A., Vanhoutte J., Copin C., Sebti Y., Derudas B., Mayi T., Bories G., Tailleux A., et al. Human Atherosclerotic Plaque Alternative Macrophages Display Low Cholesterol Handling but High Phagocytosis Because of Distinct Activities of the PPARgamma and LXRalpha Pathways. Circ. Res. 2011;108:985-995.
Not in our library10.1161/circresaha.110.233775
151.
Pirro M., Schillaci G., Savarese G., Gemelli F., Mannarino M.R., Siepi D., Bagaglia F., Mannarino E. Attenuation of inflammation with short-term dietary intervention is associated with a reduction of arterial stiffness in subjects with hypercholesterolaemia. Eur. J. Cardiovasc. Prev. Rehabil. 2004;11:497-502.
Not in our library10.1097/00149831-200412000-00009
152.
Morris D.L., Singer K., Lumeng C.N. Adipose tissue macrophages: Phenotypic plasticity and diversity in lean and obese states. Curr. Opin. Clin. Nutr. Metab. Care. 2011;14:341-346.
Not in our library10.1097/mco.0b013e328347970b
153.
Llodra J., Angeli V., Liu J., Trogan E., Fisher E.A., Randolph G.J. Emigration of monocyte-derived cells from atherosclerotic lesions characterizes regressive, but not progressive, plaques. Proc. Natl. Acad. Sci. USA. 2004;101:11779-11784.
Not in our library10.1073/pnas.0403259101
154.
Shioi A., Ikari Y. Plaque Calcification During Atherosclerosis Progression and Regression. J. Atheroscler. Thromb. 2018;25:294-303.
Not in our library10.5551/jat.rv17020
155.
Al-Sharea A., Lee M.K., Moore X.L., Fang L., Sviridov D., Chin-Dusting J., Andrews K.L., Murphy A.J. Native LDL promotes differentiation of human monocytes to macrophages with an inflammatory phenotype. Thromb Haemost. 2016;115:762-772.
Not in our library10.1160/th15-07-0571
156.
Jiang Y., Wang M., Huang K., Zhang Z., Shao N., Zhang Y., Wang W., Wang S. Oxidized low-density lipoprotein induces secretion of interleukin-1beta by macrophages via reactive oxygen species-dependent NLRP3 inflammasome activation. Biochem Biophys Res Commun. 2012;425:121-126.
Not in our library10.1016/j.bbrc.2012.07.011
157.
van Tits L.J., Stienstra R., van Lent P.L., Netea M.G., Joosten L.A., Stalenhoef A.F. Oxidized LDL enhances pro-inflammatory responses of alternatively activated M2 macrophages: A crucial role for Kruppel-like factor 2. Atherosclerosis. 2011;214:345-349.
Not in our library10.1016/j.atherosclerosis.2010.11.018
158.
Hirata Y., Tabata M., Kurobe H., Motoki T., Akaike M., Nishio C., Higashida M., Mikasa H., Nakaya Y., Takanashi S., et al. Coronary atherosclerosis is associated with macrophage polarization in epicardial adipose tissue. J. Am. Coll. Cardiol. 2011;58:248-255.
Not in our library10.1016/j.jacc.2011.01.048
159.
Hirata Y., Kurobe H., Akaike M., Chikugo F., Hori T., Bando Y., Nishio C., Higashida M., Nakaya Y., Kitagawa T., et al. Enhanced inflammation in epicardial fat in patients with coronary artery disease. Int. Heart J. 2011;52:139-142.
Not in our library10.1536/ihj.52.139
160.
Back M., Yurdagul A., Tabas I., Oorni K., Kovanen P.T. Inflammation and its resolution in atherosclerosis: Mediators and therapeutic opportunities. Nat. Rev. Cardiol. 2019;16:389-406.
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161.
Nordestgaard B.G., Wootton R., Lewis B. Selective retention of VLDL, IDL, and LDL in the arterial intima of genetically hyperlipidemic rabbits in vivo. Molecular size as a determinant of fractional loss from the intima-inner media. Arterioscler. Thromb. Vasc. Biol. 1995;15:534-542.
Not in our library10.1161/01.atv.15.4.534
162.
Shaikh M., Wootton R., Nordestgaard B.G., Baskerville P., Lumley J.S., La Ville A.E., Quiney J., Lewis B. Quantitative studies of transfer in vivo of low density, Sf 12-60, and Sf 60-400 lipoproteins between plasma and arterial intima in humans. Arterioscler. Thromb. 1991;11:569-577.
Not in our library10.1161/01.atv.11.3.569
163.
Boren J., Williams K.J. The central role of arterial retention of cholesterol-rich apolipoprotein-B-containing lipoproteins in the pathogenesis of atherosclerosis: A triumph of simplicity. Curr. Opin. Lipidol. 2016;27:473-483.
Not in our library10.1097/mol.0000000000000330
164.
Houde M., Van Eck M. Escaping the atherogenic trap: Preventing LDL fusion and binding in the intima. Atherosclerosis. 2018;275:376-378.
Not in our library10.1016/j.atherosclerosis.2018.05.032
165.
Oorni K., Pentikainen M.O., Ala-Korpela M., Kovanen P.T. Aggregation, fusion, and vesicle formation of modified low density lipoprotein particles: Molecular mechanisms and effects on matrix interactions. J. Lipid Res. 2000;41:1703-1714.
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Sheedy F.J., Grebe A., Rayner K.J., Kalantari P., Ramkhelawon B., Carpenter S.B., Becker C.E., Ediriweera H.N., Mullick A.E., Golenbock D.T., et al. CD36 coordinates NLRP3 inflammasome activation by facilitating intracellular nucleation of soluble ligands into particulate ligands in sterile inflammation. Nat. Immunol. 2013;14:812-820.
Not in our library10.1038/ni.2639
167.
Maguire E.M., Pearce S.W.A., Xiao Q. Foam cell formation: A new target for fighting atherosclerosis and cardiovascular disease. Vascul. Pharmacol. 2019;112:54-71.
Not in our library10.1016/j.vph.2018.08.002
168.
Endothelial Barrier and Its Abnormalities in Cardiovascular Disease · 2015
No notice
169.
Hutchins P.M., Heinecke J.W. Cholesterol efflux capacity, macrophage reverse cholesterol transport and cardioprotective HDL. Curr. Opin. Lipidol. 2015;26:388-393.
Not in our library10.1097/mol.0000000000000209
170.
Lao K.H., Zeng L., Xu Q. Endothelial and smooth muscle cell transformation in atherosclerosis. Curr. Opin. Lipidol. 2015;26:449-456.
Not in our library10.1097/mol.0000000000000219
171.
Chistiakov D.A., Melnichenko A.A., Myasoedova V.A., Grechko A.V., Orekhov A.N. Mechanisms of foam cell formation in atherosclerosis. J. Mol. Med. 2017;95:1153-1165.
Not in our library10.1007/s00109-017-1575-8
172.
Bobryshev Y.V. Monocyte recruitment and foam cell formation in atherosclerosis. Micron. 2006;37:208-222.
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173.
Bekkering S., Quintin J., Joosten L.A., van der Meer J.W., Netea M.G., Riksen N.P. Oxidized low-density lipoprotein induces long-term proinflammatory cytokine production and foam cell formation via epigenetic reprogramming of monocytes. Arterioscler. Thromb. Vasc. Biol. 2014;34:1731-1738.
Not in our library10.1161/atvbaha.114.303887
174.
Acton S.L., Scherer P.E., Lodish H.F., Krieger M. Expression cloning of SR-BI, a CD36-related class B scavenger receptor. J. Biol. Chem. 1994;269:21003-21009.
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175.
Endemann G., Stanton L.W., Madden K.S., Bryant C.M., White R.T., Protter A.A. CD36 is a receptor for oxidized low density lipoprotein. J. Biol. Chem. 1993;268:11811-11816.
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176.
Kodama T., Freeman M., Rohrer L., Zabrecky J., Matsudaira P., Krieger M. Type I macrophage scavenger receptor contains alpha-helical and collagen-like coiled coils. Nature. 1990;343:531-535.
Not in our library10.1038/343531a0
177.
Rahaman S.O., Lennon D.J., Febbraio M., Podrez E.A., Hazen S.L., Silverstein R.L. A CD36-dependent signaling cascade is necessary for macrophage foam cell formation. Cell Metab. 2006;4:211-221.
Not in our library10.1016/j.cmet.2006.06.007
178.
Coller S.P., Paulnock D.M. Signaling pathways initiated in macrophages after engagement of type A scavenger receptors. J. Leukoc. Biol. 2001;70:142-148.
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179.
Agrawal S., Febbraio M., Podrez E., Cathcart M.K., Stark G.R., Chisolm G.M. Signal transducer and activator of transcription 1 is required for optimal foam cell formation and atherosclerotic lesion development. Circulation. 2007;115:2939-2947.
Not in our library10.1161/circulationaha.107.696922
180.
Yu X.H., Fu Y.C., Zhang D.W., Yin K., Tang C.K. Foam cells in atherosclerosis. Clin. Chim. Acta. 2013;424:245-252.
Not in our library10.1016/j.cca.2013.06.006
181.
Kume N., Moriwaki H., Kataoka H., Minami M., Murase T., Sawamura T., Masaki T., Kita T. Inducible expression of LOX-1, a novel receptor for oxidized LDL, in macrophages and vascular smooth muscle cells. Ann. N. Y. Acad. Sci. 2000;902:323-327.
Not in our library10.1111/j.1749-6632.2000.tb06332.x
182.
Ghosh S. Early steps in reverse cholesterol transport: Cholesteryl ester hydrolase and other hydrolases. Curr. Opin. Endocrinol. Diabetes Obes. 2012;19:136-141.
Not in our library10.1097/med.0b013e3283507836
183.
Macrophage‐mediated cholesterol handling in atherosclerosis · 2015
No notice
184.
Favari E., Chroni A., Tietge U.J., Zanotti I., Escola-Gil J.C., Bernini F. Cholesterol efflux and reverse cholesterol transport. Handb. Exp. Pharmacol. 2015;224:181-206.
Not in our library10.1007/978-3-319-09665-0_4
185.
da Silva R.F., Lappalainen J., Lee-Rueckert M., Kovanen P.T. Conversion of human M-CSF macrophages into foam cells reduces their proinflammatory responses to classical M1-polarizing activation. Atherosclerosis. 2016;248:170-178.
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186.
Li Y.B., Zhang Q.H., Chen Z., He Z.J., Yi G.H. Oxidized low-density lipoprotein attenuated desmoglein 1 and desmocollin 2 expression via LOX-1/Ca(2+)/PKC-beta signal in human umbilical vein endothelial cells. Biochem. Biophys. Res. Commun. 2015;468:380-386.
Not in our library10.1016/j.bbrc.2015.10.079
187.
van Nieuw Amerongen G.P., Vermeer M.A., Negre-Aminou P., Lankelma J., Emeis J.J., van Hinsbergh V.W. Simvastatin improves disturbed endothelial barrier function. Circulation. 2000;102:2803-2809.
Not in our library10.1161/01.cir.102.23.2803
188.
Kasa A., Csortos C., Verin A.D. Cytoskeletal mechanisms regulating vascular endothelial barrier function in response to acute lung injury. Tissue Barriers. 2015;3:e974448.
Not in our library10.4161/21688370.2014.974448
189.
Syed S.E., Trinnaman B., Martin S., Major S., Hutchinson J., Magee A.I. Molecular interactions between desmosomal cadherins. Biochem. J. 2002;362:317-327.
Not in our library10.1042/bj3620317
190.
Ben J., Zhu X., Zhang H., Chen Q. Class A1 scavenger receptors in cardiovascular diseases. Br. J. Pharmacol. 2015;172:5523-5530.
Not in our library10.1111/bph.13105
191.
Murphy J.E., Tedbury P.R., Homer-Vanniasinkam S., Walker J.H., Ponnambalam S. Biochemistry and cell biology of mammalian scavenger receptors. Atherosclerosis. 2005;182:1-15.
Not in our library10.1016/j.atherosclerosis.2005.03.036
192.
Moore K.J., Freeman M.W. Scavenger receptors in atherosclerosis: Beyond lipid uptake. Arterioscler. Thromb. Vasc. Biol. 2006;26:1702-1711.
Not in our library10.1161/01.atv.0000229218.97976.43
193.
Makinen P.I., Lappalainen J.P., Heinonen S.E., Leppanen P., Lahteenvuo M.T., Aarnio J.V., Heikkila J., Turunen M.P., Yla-Herttuala S. Silencing of either SR-A or CD36 reduces atherosclerosis in hyperlipidaemic mice and reveals reciprocal upregulation of these receptors. Cardiovasc. Res. 2010;88:530-538.
Not in our library10.1093/cvr/cvq235
194.
Dai X.Y., Cai Y., Mao D.D., Qi Y.F., Tang C., Xu Q., Zhu Y., Xu M.J., Wang X. Increased stability of phosphatase and tensin homolog by intermedin leading to scavenger receptor A inhibition of macrophages reduces atherosclerosis in apolipoprotein E-deficient mice. J. Mol. Cell. Cardiol. 2012;53:509-520.
Not in our library10.1016/j.yjmcc.2012.07.006
195.
Suzuki H., Kurihara Y., Takeya M., Kamada N., Kataoka M., Jishage K., Ueda O., Sakaguchi H., Higashi T., Suzuki T., et al. A role for macrophage scavenger receptors in atherosclerosis and susceptibility to infection. Nature. 1997;386:292-296.
Not in our library10.1038/386292a0
196.
Sakaguchi H., Takeya M., Suzuki H., Hakamata H., Kodama T., Horiuchi S., Gordon S., van der Laan L.J., Kraal G., Ishibashi S., et al. Role of macrophage scavenger receptors in diet-induced atherosclerosis in mice. Lab. Investig. 1998;78:423-434.
Not in our library
197.
Babaev V.R., Gleaves L.A., Carter K.J., Suzuki H., Kodama T., Fazio S., Linton M.F. Reduced atherosclerotic lesions in mice deficient for total or macrophage-specific expression of scavenger receptor-A. Arterioscler. Thromb. Vasc. Biol. 2000;20:2593-2599.
Not in our library10.1161/01.atv.20.12.2593
198.
Hashizume M., Mihara M. Blockade of IL-6 and TNF-alpha inhibited oxLDL-induced production of MCP-1 via scavenger receptor induction. Eur. J. Pharmacol. 2012;689:249-254.
Not in our library10.1016/j.ejphar.2012.05.035
199.
Zhao J.F., Ching L.C., Huang Y.C., Chen C.Y., Chiang A.N., Kou Y.R., Shyue S.K., Lee T.S. Molecular mechanism of curcumin on the suppression of cholesterol accumulation in macrophage foam cells and atherosclerosis. Mol. Nutr. Food Res. 2012;56:691-701.
Not in our library10.1002/mnfr.201100735
200.
Van Berkel T.J., Van Eck M., Herijgers N., Fluiter K., Nion S. Scavenger receptor classes A and B. Their roles in atherogenesis and the metabolism of modified LDL and HDL. Ann. N. Y. Acad. Sci. 2000;902:113-126.
Not in our library10.1111/j.1749-6632.2000.tb06306.x
201.
Pepino M.Y., Kuda O., Samovski D., Abumrad N.A. Structure-function of CD36 and importance of fatty acid signal transduction in fat metabolism. Annu. Rev. Nutr. 2014;34:281-303.
Not in our library10.1146/annurev-nutr-071812-161220
202.
Stewart C.R., Stuart L.M., Wilkinson K., van Gils J.M., Deng J., Halle A., Rayner K.J., Boyer L., Zhong R., Frazier W.A., et al. CD36 ligands promote sterile inflammation through assembly of a Toll-like receptor 4 and 6 heterodimer. Nat. Immunol. 2010;11:155-161.
Not in our library10.1038/ni.1836
203.
Parsons M.S., Barrett L., Little C., Grant M.D. Harnessing CD36 to rein in inflammation. Endocr. Metab. Immune Disord. Drug Targets. 2008;8:184-191.
Not in our library10.2174/187153008785700073
204.
Hrboticky N., Draude G., Hapfelmeier G., Lorenz R., Weber P.C. Lovastatin decreases the receptor-mediated degradation of acetylated and oxidized LDLs in human blood monocytes during the early stage of differentiation into macrophages. Arterioscler. Thromb. Vasc. Biol. 1999;19:1267-1275.
Not in our library10.1161/01.atv.19.5.1267
205.
Fuhrman B., Koren L., Volkova N., Keidar S., Hayek T., Aviram M. Atorvastatin therapy in hypercholesterolemic patients suppresses cellular uptake of oxidized-LDL by differentiating monocytes. Atherosclerosis. 2002;164:179-185.
Not in our library10.1016/s0021-9150(02)00063-1
206.
Geloen A., Helin L., Geeraert B., Malaud E., Holvoet P., Marguerie G. CD36 inhibitors reduce postprandial hypertriglyceridemia and protect against diabetic dyslipidemia and atherosclerosis. PLoS ONE. 2012;7:e37633.
Not in our library10.1371/journal.pone.0037633
207.
Mansor L.S., Sousa Fialho M.D.L., Yea G., Coumans W.A., West J.A., Kerr M., Carr C.A., Luiken J., Glatz J.F.C., Evans R.D., et al. Inhibition of sarcolemmal FAT/CD36 by sulfo-N-succinimidyl oleate rapidly corrects metabolism and restores function in the diabetic heart following hypoxia/reoxygenation. Cardiovasc. Res. 2017;113:737-748.
Not in our library10.1093/cvr/cvx045
208.
Expression of the Receptor Tyrosine Kinase EphB2 on Dendritic Cells Is Modulated by Toll-Like Receptor Ligation but Is Not Required for T Cell Activation. · 2015
Not checked
209.
Li L., Sawamura T., Renier G. Glucose enhances human macrophage LOX-1 expression: Role for LOX-1 in glucose-induced macrophage foam cell formation. Circ. Res. 2004;94:892-901.
Not in our library10.1161/01.res.0000124920.09738.26
210.
Gao D., Pararasa C., Dunston C.R., Bailey C.J., Griffiths H.R. Palmitate promotes monocyte atherogenicity via de novo ceramide synthesis. Free Radic. Biol. Med. 2012;53:796-806.
Not in our library10.1016/j.freeradbiomed.2012.05.026
211.
Li X.Y., Wang C., Xiang X.R., Chen F.C., Yang C.M., Wu J. Porphyromonas gingivalis lipopolysaccharide increases lipid accumulation by affecting CD36 and ATP-binding cassette transporter A1 in macrophages. Oncol. Rep. 2013;30:1329-1336.
Not in our library10.3892/or.2013.2600
212.
Choi J.S., Bae J.Y., Kim D.S., Li J., Kim J.L., Lee Y.J., Kang Y.H. Dietary compound quercitrin dampens VEGF induction and PPARgamma activation in oxidized LDL-exposed murine macrophages: Association with scavenger receptor CD36. J. Agric. Food Chem. 2010;58:1333-1341.
Not in our library10.1021/jf9032443
213.
Tang F.T., Cao Y., Wang T.Q., Wang L.J., Guo J., Zhou X.S., Xu S.W., Liu W.H., Liu P.Q., Huang H.Q. Tanshinone IIA attenuates atherosclerosis in ApoE(-/-) mice through down-regulation of scavenger receptor expression. Eur. J. Pharmacol. 2011;650:275-284.
Not in our library10.1016/j.ejphar.2010.07.038
214.
Granados-Principal S., Quiles J.L., Ramirez-Tortosa C.L., Ochoa-Herrera J., Perez-Lopez P., Pulido-Moran M., Ramirez-Tortosa M.C. Squalene ameliorates atherosclerotic lesions through the reduction of CD36 scavenger receptor expression in macrophages. Mol. Nutr. Food Res. 2012;56:733-740.
Not in our library10.1002/mnfr.201100703
215.
Febbraio M., Podrez E.A., Smith J.D., Hajjar D.P., Hazen S.L., Hoff H.F., Sharma K., Silverstein R.L. Targeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice. J. Clin. Investig. 2000;105:1049-1056.
Not in our library10.1172/jci9259
216.
Moore K.J., Kunjathoor V.V., Koehn S.L., Manning J.J., Tseng A.A., Silver J.M., McKee M., Freeman M.W. Loss of receptor-mediated lipid uptake via scavenger receptor A or CD36 pathways does not ameliorate atherosclerosis in hyperlipidemic mice. J. Clin. Investig. 2005;115:2192-2201.
Not in our library10.1172/jci24061
217.
Kataoka H., Kume N., Miyamoto S., Minami M., Moriwaki H., Murase T., Sawamura T., Masaki T., Hashimoto N., Kita T. Expression of lectinlike oxidized low-density lipoprotein receptor-1 in human atherosclerotic lesions. Circulation. 1999;99:3110-3117.
Not in our library10.1161/01.cir.99.24.3110
218.
Schaeffer D.F., Riazy M., Parhar K.S., Chen J.H., Duronio V., Sawamura T., Steinbrecher U.P. LOX-1 augments oxLDL uptake by lysoPC-stimulated murine macrophages but is not required for oxLDL clearance from plasma. J. Lipid Res. 2009;50:1676-1684.
Not in our library10.1194/jlr.m900167-jlr200
219.
LOX-1, OxLDL, and Atherosclerosis · 2013
No notice
220.
Inoue K., Arai Y., Kurihara H., Kita T., Sawamura T. Overexpression of lectin-like oxidized low-density lipoprotein receptor-1 induces intramyocardial vasculopathy in apolipoprotein E-null mice. Circ. Res. 2005;97:176-184.
Not in our library10.1161/01.res.0000174286.73200.d4
221.
Ding Z., Liu S., Wang X., Deng X., Fan Y., Shahanawaz J., Shmookler Reis R.J., Varughese K.I., Sawamura T., Mehta J.L. Cross-talk between LOX-1 and PCSK9 in vascular tissues. Cardiovasc. Res. 2015;107:556-567.
Not in our library10.1093/cvr/cvv178
222.
Ishino S., Mukai T., Kume N., Asano D., Ogawa M., Kuge Y., Minami M., Kita T., Shiomi M., Saji H. Lectin-like oxidized LDL receptor-1 (LOX-1) expression is associated with atherosclerotic plaque instability--analysis in hypercholesterolemic rabbits. Atherosclerosis. 2007;195:48-56.
Not in our library10.1016/j.atherosclerosis.2006.11.031
223.
Kuge Y., Kume N., Ishino S., Takai N., Ogawa Y., Mukai T., Minami M., Shiomi M., Saji H. Prominent lectin-like oxidized low density lipoprotein (LDL) receptor-1 (LOX-1) expression in atherosclerotic lesions is associated with tissue factor expression and apoptosis in hypercholesterolemic rabbits. Biol. Pharm. Bull. 2008;31:1475-1482.
Not in our library10.1248/bpb.31.1475
224.
Fazio S., Major A.S., Swift L.L., Gleaves L.A., Accad M., Linton M.F., Farese R.V. Increased atherosclerosis in LDL receptor-null mice lacking ACAT1 in macrophages. J. Clin. Investig. 2001;107:163-171.
Not in our library10.1172/jci10310
225.
Accad M., Smith S.J., Newland D.L., Sanan D.A., King L.E., Linton M.F., Fazio S., Farese R.V. Massive xanthomatosis and altered composition of atherosclerotic lesions in hyperlipidemic mice lacking acyl CoA:cholesterol acyltransferase 1. J. Clin. Investig. 2000;105:711-719.
Not in our library10.1172/jci9021
226.
Perrey S., Legendre C., Matsuura A., Guffroy C., Binet J., Ohbayashi S., Tanaka T., Ortuno J.C., Matsukura T., Laugel T., et al. Preferential pharmacological inhibition of macrophage ACAT increases plaque formation in mouse and rabbit models of atherogenesis. Atherosclerosis. 2001;155:359-370.
Not in our library10.1016/s0021-9150(00)00599-2
227.
Chang C.C., Sakashita N., Ornvold K., Lee O., Chang E.T., Dong R., Lin S., Lee C.Y., Strom S.C., Kashyap R., et al. Immunological quantitation and localization of ACAT-1 and ACAT-2 in human liver and small intestine. J. Biol. Chem. 2000;275:28083-28092.
Not in our library10.1074/jbc.m003927200
228.
Cheng B., Wan J., Wang Y., Mei C., Liu W., Ke L., He P. Ghrelin inhibits foam cell formation via simultaneously down-regulating the expression of acyl-coenzyme A:cholesterol acyltransferase 1 and up-regulating adenosine triphosphate-binding cassette transporter A1. Cardiovasc. Pathol. 2010;19:e159-e166.
Not in our library10.1016/j.carpath.2009.07.001
229.
Nagashima M., Watanabe T., Terasaki M., Tomoyasu M., Nohtomi K., Kim-Kaneyama J., Miyazaki A., Hirano T. Native incretins prevent the development of atherosclerotic lesions in apolipoprotein E knockout mice. Diabetologia. 2011;54:2649-2659.
Not in our library10.1007/s00125-011-2241-2
230.
Darsalia V., Larsson M., Klein T., Patrone C. The high need for trials assessing functional outcome after stroke rather than stroke prevention with GLP-1 agonists and DPP-4 inhibitors. Cardiovasc. Diabetol. 2018;17:32.
Not in our library10.1186/s12933-018-0674-3
231.
Ge J., Zhai W., Cheng B., He P., Qi B., Lu H., Zeng Y., Chen X. Insulin induces human acyl-coenzyme A: Cholesterol acyltransferase1 gene expression via MAP kinases and CCAAT/enhancer-binding protein alpha. J. Cell. Biochem. 2013;114:2188-2198.
Not in our library10.1002/jcb.24568
232.
Hongo S., Watanabe T., Arita S., Kanome T., Kageyama H., Shioda S., Miyazaki A. Leptin modulates ACAT1 expression and cholesterol efflux from human macrophages. Am. J. Physiol. Endocrinol. Metab. 2009;297:E474-E482.
Not in our library10.1152/ajpendo.90369.2008
233.
Targeting of neutral cholesterol ester hydrolase to the endoplasmic reticulum via its N-terminal sequence[S] · 2010
Not checked
234.
Zhao B., Song J., Chow W.N., St Clair R.W., Rudel L.L., Ghosh S. Macrophage-specific transgenic expression of cholesteryl ester hydrolase significantly reduces atherosclerosis and lesion necrosis in Ldlr mice. J. Clin. Investig. 2007;117:2983-2992.
Not in our library10.1172/jci30485
235.
Igarashi M., Osuga J., Uozaki H., Sekiya M., Nagashima S., Takahashi M., Takase S., Takanashi M., Li Y., Ohta K., et al. The critical role of neutral cholesterol ester hydrolase 1 in cholesterol removal from human macrophages. Circ. Res. 2010;107:1387-1395.
Not in our library10.1161/circresaha.110.226613
236.
Sekiya M., Osuga J., Nagashima S., Ohshiro T., Igarashi M., Okazaki H., Takahashi M., Tazoe F., Wada T., Ohta K., et al. Ablation of neutral cholesterol ester hydrolase 1 accelerates atherosclerosis. Cell Metab. 2009;10:219-228.
Not in our library10.1016/j.cmet.2009.08.004
237.
Critical role of neutral cholesteryl ester hydrolase 1 in cholesteryl ester hydrolysis in murine macrophages[S] · 2014
Not checked
238.
Sekiya M., Osuga J., Igarashi M., Okazaki H., Ishibashi S. The role of neutral cholesterol ester hydrolysis in macrophage foam cells. J. Atheroscler Thromb. 2011;18:359-364.
Not in our library10.5551/jat.7013
239.
Zhao Y., Pennings M., Vrins C.L., Calpe-Berdiel L., Hoekstra M., Kruijt J.K., Ottenhoff R., Hildebrand R.B., van der Sluis R., Jessup W., et al. Hypocholesterolemia, foam cell accumulation, but no atherosclerosis in mice lacking ABC-transporter A1 and scavenger receptor BI. Atherosclerosis. 2011;218:314-322.
Not in our library10.1016/j.atherosclerosis.2011.07.096
240.
Joyce C.W., Wagner E.M., Basso F., Amar M.J., Freeman L.A., Shamburek R.D., Knapper C.L., Syed J., Wu J., Vaisman B.L., et al. ABCA1 overexpression in the liver of LDLr-KO mice leads to accumulation of pro-atherogenic lipoproteins and enhanced atherosclerosis. J. Biol. Chem. 2006;281:33053-33065.
Not in our library10.1074/jbc.m604526200
241.
Baldan A., Pei L., Lee R., Tarr P., Tangirala R.K., Weinstein M.M., Frank J., Li A.C., Tontonoz P., Edwards P.A. Impaired development of atherosclerosis in hyperlipidemic Ldlr-/- and ApoE-/- mice transplanted with Abcg1-/- bone marrow. Arterioscler. Thromb. Vasc. Biol. 2006;26:2301-2307.
Not in our library10.1161/01.atv.0000240051.22944.dc
242.
Meurs I., Lammers B., Zhao Y., Out R., Hildebrand R.B., Hoekstra M., Van Berkel T.J., Van Eck M. The effect of ABCG1 deficiency on atherosclerotic lesion development in LDL receptor knockout mice depends on the stage of atherogenesis. Atherosclerosis. 2012;221:41-47.
Not in our library10.1016/j.atherosclerosis.2011.11.024
243.
Zhang W., Yancey P.G., Su Y.R., Babaev V.R., Zhang Y., Fazio S., Linton M.F. Inactivation of macrophage scavenger receptor class B type I promotes atherosclerotic lesion development in apolipoprotein E-deficient mice. Circulation. 2003;108:2258-2263.
Not in our library10.1161/01.cir.0000093189.97429.9d
244.
Bennett D.J., Cooke A.J., Edwards A.S. Non-steroidal LXR agonists; an emerging therapeutic strategy for the treatment of atherosclerosis. Recent Pat. Cardiovasc. Drug Discov. 2006;1:21-46.
Not in our library10.2174/157489006775244245
245.
Lee S.M., Moon J., Cho Y., Chung J.H., Shin M.J. Quercetin up-regulates expressions of peroxisome proliferator-activated receptor gamma, liver X receptor alpha, and ATP binding cassette transporter A1 genes and increases cholesterol efflux in human macrophage cell line. Nutr. Res. 2013;33:136-143.
Not in our library10.1016/j.nutres.2012.11.010
246.
Ogura M., Ayaori M., Terao Y., Hisada T., Iizuka M., Takiguchi S., Uto-Kondo H., Yakushiji E., Nakaya K., Sasaki M., et al. Proteasomal inhibition promotes ATP-binding cassette transporter A1 (ABCA1) and ABCG1 expression and cholesterol efflux from macrophages in vitro and in vivo. Arterioscler. Thromb. Vasc. Biol. 2011;31:1980-1987.
Not in our library10.1161/atvbaha.111.228478
247.
Tang C.K., Tang G.H., Yi G.H., Wang Z., Liu L.S., Wan S., Yuan Z.H., He X.S., Yang J.H., Ruan C.G., et al. Effect of apolipoprotein A-I on ATP binding cassette transporter A1 degradation and cholesterol efflux in THP-1 macrophage-derived foam cells. Acta Biochim. Biophys. Sin. (Shanghai). 2004;36:218-226.
Not in our library10.1093/abbs/36.3.218
248.
Rousselle A., Qadri F., Leukel L., Yilmaz R., Fontaine J.F., Sihn G., Bader M., Ahluwalia A., Duchene J. CXCL5 limits macrophage foam cell formation in atherosclerosis. J. Clin. Investig. 2013;123:1343-1347.
Not in our library10.1172/jci66580
249.
Santamarina-Fojo S., Remaley A.T., Neufeld E.B., Brewer H.B. Regulation and intracellular trafficking of the ABCA1 transporter. J. Lipid Res. 2001;42:1339-1345.
Not in our library
250.
Wang Y., Oram J.F. Unsaturated fatty acids phosphorylate and destabilize ABCA1 through a protein kinase C delta pathway. J. Lipid Res. 2007;48:1062-1068.
Not in our library10.1194/jlr.m600437-jlr200
251.
Ku C.S., Park Y., Coleman S.L., Lee J. Unsaturated fatty acids repress expression of ATP binding cassette transporter A1 and G1 in RAW 264.7 macrophages. J. Nutr. Biochem. 2012;23:1271-1276.
Not in our library10.1016/j.jnutbio.2011.07.007
252.
Yu X.H., Jiang H.L., Chen W.J., Yin K., Zhao G.J., Mo Z.C., Ouyang X.P., Lv Y.C., Jiang Z.S., Zhang D.W., et al. Interleukin-18 and interleukin-12 together downregulate ATP-binding cassette transporter A1 expression through the interleukin-18R/nuclear factor-kappaB signaling pathway in THP-1 macrophage-derived foam cells. Circ. J. 2012;76:1780-1791.
Not in our library10.1253/circj.cj-11-1338
253.
Jun H.J., Hoang M.H., Yeo S.K., Jia Y., Lee S.J. Induction of ABCA1 and ABCG1 expression by the liver X receptor modulator cineole in macrophages. Bioorg Med. Chem. Lett. 2013;23:579-583.
Not in our library10.1016/j.bmcl.2012.11.012
254.
Helal O., Berrougui H., Loued S., Khalil A. Extra-virgin olive oil consumption improves the capacity of HDL to mediate cholesterol efflux and increases ABCA1 and ABCG1 expression in human macrophages. Br. J. Nutr. 2013;109:1844-1855.
Not in our library10.1017/s0007114512003856
255.
Wang D., Xia M., Yan X., Li D., Wang L., Xu Y., Jin T., Ling W. Gut microbiota metabolism of anthocyanin promotes reverse cholesterol transport in mice via repressing miRNA-10b. Circ. Res. 2012;111:967-981.
Not in our library10.1161/circresaha.112.266502
256.
Uto-Kondo H., Ayaori M., Ogura M., Nakaya K., Ito M., Suzuki A., Takiguchi S., Yakushiji E., Terao Y., Ozasa H., et al. Coffee consumption enhances high-density lipoprotein-mediated cholesterol efflux in macrophages. Circ. Res. 2010;106:779-787.
Not in our library10.1161/circresaha.109.206615
257.
Kammerer I., Ringseis R., Biemann R., Wen G., Eder K. 13-hydroxy linoleic acid increases expression of the cholesterol transporters ABCA1, ABCG1 and SR-BI and stimulates apoA-I-dependent cholesterol efflux in RAW264.7 macrophages. Lipids Health Dis. 2011;10:222.
Not in our library10.1186/1476-511x-10-222
258.
Voloshyna I., Hai O., Littlefield M.J., Carsons S., Reiss A.B. Resveratrol mediates anti-atherogenic effects on cholesterol flux in human macrophages and endothelium via PPARgamma and adenosine. Eur. J. Pharmacol. 2013;698:299-309.
Not in our library10.1016/j.ejphar.2012.08.024
259.
Tang S.L., Chen W.J., Yin K., Zhao G.J., Mo Z.C., Lv Y.C., Ouyang X.P., Yu X.H., Kuang H.J., Jiang Z.S., et al. PAPP-A negatively regulates ABCA1, ABCG1 and SR-B1 expression by inhibiting LXRalpha through the IGF-I-mediated signaling pathway. Atherosclerosis. 2012;222:344-354.
Not in our library10.1016/j.atherosclerosis.2012.03.005
260.
Duewell P., Kono H., Rayner K.J., Sirois C.M., Vladimer G., Bauernfeind F.G., Abela G.S., Franchi L., Nunez G., Schnurr M., et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature. 2010;464:1357-1361.
Not in our library10.1038/nature08938
261.
Libby P., Aikawa M., Schonbeck U. Cholesterol and atherosclerosis. Biochim. Biophys. Acta. 2000;1529:299-309.
Not in our library10.1016/s1388-1981(00)00161-x
262.
Sottero B., Gamba P., Longhi M., Robbesyn F., Abuja P.M., Schaur R.J., Poli G., Leonarduzzi G. Expression and synthesis of TGFbeta1 is induced in macrophages by 9-oxononanoyl cholesterol, a major cholesteryl ester oxidation product. Biofactors. 2005;24:209-216.
Not in our library10.1002/biof.5520240125
263.
McCarthy C., Duffy M.M., Mooney D., James W.G., Griffin M.D., Fitzgerald D.J., Belton O. IL-10 mediates the immunoregulatory response in conjugated linoleic acid-induced regression of atherosclerosis. FASEB J. 2013;27:499-510.
Not in our library10.1096/fj.12-215442
264.
Banchereau J., Briere F., Caux C., Davoust J., Lebecque S., Liu Y.J., Pulendran B., Palucka K. Immunobiology of dendritic cells. Annu. Rev. Immunol. 2000;18:767-811.
Not in our library10.1146/annurev.immunol.18.1.767
265.
Zernecke A. Dendritic cells in atherosclerosis: Evidence in mice and humans. Arterioscler. Thromb. Vasc. Biol. 2015;35:763-770.
Not in our library10.1161/atvbaha.114.303566
266.
Bousso P. T-cell activation by dendritic cells in the lymph node: Lessons from the movies. Nat. Rev. Immunol. 2008;8:675-684.
Not in our library10.1038/nri2379
267.
Steinman R.M. Decisions about dendritic cells: Past, present, and future. Annu. Rev. Immunol. 2012;30:1-22.
Not in our library10.1146/annurev-immunol-100311-102839
268.
Schraml B.U., Reis e Sousa C. Defining dendritic cells. Curr. Opin. Immunol. 2015;32:13-20.
Not in our library10.1016/j.coi.2014.11.001
269.
Mildner A., Jung S. Development and function of dendritic cell subsets. Immunity. 2014;40:642-656.
Not in our library10.1016/j.immuni.2014.04.016
270.
Guilliams M., Dutertre C.A., Scott C.L., McGovern N., Sichien D., Chakarov S., Van Gassen S., Chen J., Poidinger M., De Prijck S., et al. Unsupervised High-Dimensional Analysis Aligns Dendritic Cells across Tissues and Species. Immunity. 2016;45:669-684.
Not in our library10.1016/j.immuni.2016.08.015
271.
Dutertre C.A., Wang L.F., Ginhoux F. Aligning bona fide dendritic cell populations across species. Cell. Immunol. 2014;291:3-10.
Not in our library10.1016/j.cellimm.2014.08.006
272.
Greter M., Helft J., Chow A., Hashimoto D., Mortha A., Agudo-Cantero J., Bogunovic M., Gautier E.L., Miller J., Leboeuf M., et al. GM-CSF controls nonlymphoid tissue dendritic cell homeostasis but is dispensable for the differentiation of inflammatory dendritic cells. Immunity. 2012;36:1031-1046.
Not in our library10.1016/j.immuni.2012.03.027
273.
Ushach I., Zlotnik A. Biological role of granulocyte macrophage colony-stimulating factor (GM-CSF) and macrophage colony-stimulating factor (M-CSF) on cells of the myeloid lineage. J. Leukoc. Biol. 2016;100:481-489.
Not in our library10.1189/jlb.3ru0316-144r
274.
Hume D.A. Macrophages as APC and the dendritic cell myth. J. Immunol. 2008;181:5829-5835.
Not in our library10.4049/jimmunol.181.9.5829
275.
Jongstra-Bilen J., Haidari M., Zhu S.N., Chen M., Guha D., Cybulsky M.I. Low-grade chronic inflammation in regions of the normal mouse arterial intima predisposed to atherosclerosis. J. Exp. Med. 2006;203:2073-2083.
Not in our library10.1084/jem.20060245
276.
Paulson K.E., Zhu S.N., Chen M., Nurmohamed S., Jongstra-Bilen J., Cybulsky M.I. Resident intimal dendritic cells accumulate lipid and contribute to the initiation of atherosclerosis. Circ. Res. 2010;106:383-390.
Not in our library10.1161/circresaha.109.210781
277.
Choi J.H., Cheong C., Dandamudi D.B., Park C.G., Rodriguez A., Mehandru S., Velinzon K., Jung I.H., Yoo J.Y., Oh G.T., et al. Flt3 signaling-dependent dendritic cells protect against atherosclerosis. Immunity. 2011;35:819-831.
Not in our library10.1016/j.immuni.2011.09.014
278.
Choi J.H., Do Y., Cheong C., Koh H., Boscardin S.B., Oh Y.S., Bozzacco L., Trumpfheller C., Park C.G., Steinman R.M. Identification of antigen-presenting dendritic cells in mouse aorta and cardiac valves. J. Exp. Med. 2009;206:497-505.
Not in our library10.1084/jem.20082129
279.
Roufaiel M., Gracey E., Siu A., Zhu S.N., Lau A., Ibrahim H., Althagafi M., Tai K., Hyduk S.J., Cybulsky K.O., et al. CCL19-CCR7-dependent reverse transendothelial migration of myeloid cells clears Chlamydia muridarum from the arterial intima. Nat. Immunol. 2016;17:1263-1272.
Not in our library10.1038/ni.3564
280.
Trogan E., Feig J.E., Dogan S., Rothblat G.H., Angeli V., Tacke F., Randolph G.J., Fisher E.A. Gene expression changes in foam cells and the role of chemokine receptor CCR7 during atherosclerosis regression in ApoE-deficient mice. Proc. Natl. Acad. Sci. USA. 2006;103:3781-3786.
Not in our library10.1073/pnas.0511043103
281.
Ginhoux F., Jung S. Monocytes and macrophages: Developmental pathways and tissue homeostasis. Nat. Rev. Immunol. 2014;14:392-404.
Not in our library10.1038/nri3671
282.
Rescigno M., Martino M., Sutherland C.L., Gold M.R., Ricciardi-Castagnoli P. Dendritic cell survival and maturation are regulated by different signaling pathways. J. Exp. Med. 1998;188:2175-2180.
Not in our library10.1084/jem.188.11.2175
283.
Pflicke H., Sixt M. Preformed portals facilitate dendritic cell entry into afferent lymphatic vessels. J. Exp. Med. 2009;206:2925-2935.
Not in our library10.1084/jem.20091739
284.
Gonzalez S.F., Lukacs-Kornek V., Kuligowski M.P., Pitcher L.A., Degn S.E., Kim Y.A., Cloninger M.J., Martinez-Pomares L., Gordon S., Turley S.J., et al. Capture of influenza by medullary dendritic cells via SIGN-R1 is essential for humoral immunity in draining lymph nodes. Nat. Immunol. 2010;11:427-434.
Not in our library10.1038/ni.1856
285.
MacRitchie N., Grassia G., Noonan J., Cole J.E., Hughes C.E., Schroeder J., Benson R.A., Cochain C., Zernecke A., Guzik T.J., et al. The aorta can act as a site of naive CD4+ T cell priming. Cardiovasc Res. 2019.
Not in our library10.1093/cvr/cvz102
286.
Weber C., Meiler S., Doring Y., Koch M., Drechsler M., Megens R.T., Rowinska Z., Bidzhekov K., Fecher C., Ribechini E., et al. CCL17-expressing dendritic cells drive atherosclerosis by restraining regulatory T cell homeostasis in mice. J. Clin. Investig. 2011;121:2898-2910.
Not in our library10.1172/jci44925
287.
Koltsova E.K., Garcia Z., Chodaczek G., Landau M., McArdle S., Scott S.R., von Vietinghoff S., Galkina E., Miller Y.I., Acton S.T., et al. Dynamic T cell-APC interactions sustain chronic inflammation in atherosclerosis. J. Clin. Investig. 2012;122:3114-3126.
Not in our library10.1172/jci61758
288.
Sun J., Hartvigsen K., Chou M.Y., Zhang Y., Sukhova G.K., Zhang J., Lopez-Ilasaca M., Diehl C.J., Yakov N., Harats D., et al. Deficiency of antigen-presenting cell invariant chain reduces atherosclerosis in mice. Circulation. 2010;122:808-820.
Not in our library10.1161/circulationaha.109.891887
289.
Wigren M., Rattik S., Yao Mattisson I., Tomas L., Gronberg C., Soderberg I., Alm R., Sundius L., Ljungcrantz I., Bjorkbacka H., et al. Lack of Ability to Present Antigens on Major Histocompatibility Complex Class II Molecules Aggravates Atherosclerosis in ApoE(-/-) Mice. Circulation. 2019;139:2554-2566.
Not in our library10.1161/circulationaha.118.039288
290.
Subramanian M., Thorp E., Hansson G.K., Tabas I. Treg-mediated suppression of atherosclerosis requires MYD88 signaling in DCs. J. Clin. Investig. 2013;123:179-188.
Not in our library10.1172/jci64617
291.
Loschko J., Schreiber H.A., Rieke G.J., Esterhazy D., Meredith M.M., Pedicord V.A., Yao K.H., Caballero S., Pamer E.G., Mucida D., et al. Absence of MHC class II on cDCs results in microbial-dependent intestinal inflammation. J. Exp. Med. 2016;213:517-534.
Not in our library10.1084/jem.20160062
292.
Agouridis A.P., Elisaf M., Milionis H.J. An overview of lipid abnormalities in patients with inflammatory bowel disease. Ann. Gastroenterol. 2011;24:181-187.
Not in our library
293.
Lievens D., Habets K.L., Robertson A.K., Laouar Y., Winkels H., Rademakers T., Beckers L., Wijnands E., Boon L., Mosaheb M., et al. Abrogated transforming growth factor beta receptor II (TGFbetaRII) signalling in dendritic cells promotes immune reactivity of T cells resulting in enhanced atherosclerosis. Eur. Heart J. 2013;34:3717-3727.
Not in our library10.1093/eurheartj/ehs106
294.
Chaudhari S.M., Sluimer J.C., Koch M., Theelen T.L., Manthey H.D., Busch M., Caballero-Franco C., Vogel F., Cochain C., Pelisek J., et al. Deficiency of HIF1alpha in Antigen-Presenting Cells Aggravates Atherosclerosis and Type 1 T-Helper Cell Responses in Mice. Arterioscler. Thromb. Vasc. Biol. 2015;35:2316-2325.
Not in our library10.1161/atvbaha.115.306171
295.
Alberts-Grill N., Engelbertsen D., Bu D., Foks A., Grabie N., Herter J.M., Kuperwaser F., Chen T., Destefano G., Jarolim P., et al. Dendritic Cell KLF2 Expression Regulates T Cell Activation and Proatherogenic Immune Responses. J. Immunol. 2016;197:4651-4662.
Not in our library10.4049/jimmunol.1600206
296.
Thomson A.W., Robbins P.D. Tolerogenic dendritic cells for autoimmune disease and transplantation. Ann. Rheum. Dis. 2008;67(Suppl. 3):iii90-iii96.
Not in our library10.1136/ard.2008.099176
297.
Mok M.Y. Tolerogenic dendritic cells: Role and therapeutic implications in systemic lupus erythematosus. Int. J. Rheum. Dis. 2015;18:250-259.
Not in our library10.1111/1756-185x.12532
298.
Habets K.L., van Puijvelde G.H., van Duivenvoorde L.M., van Wanrooij E.J., de Vos P., Tervaert J.W., van Berkel T.J., Toes R.E., Kuiper J. Vaccination using oxidized low-density lipoprotein-pulsed dendritic cells reduces atherosclerosis in LDL receptor-deficient mice. Cardiovasc. Res. 2010;85:622-630.
Not in our library10.1093/cvr/cvp338
299.
Hermansson A., Johansson D.K., Ketelhuth D.F., Andersson J., Zhou X., Hansson G.K. Immunotherapy with tolerogenic apolipoprotein B-100-loaded dendritic cells attenuates atherosclerosis in hypercholesterolemic mice. Circulation. 2011;123:1083-1091.
Not in our library10.1161/circulationaha.110.973222
300.
Rombouts M., Cools N., Grootaert M.O., de Bakker F., Van Brussel I., Wouters A., De Meyer G.R., De Winter B.Y., Schrijvers D.M. Long-Term Depletion of Conventional Dendritic Cells Cannot Be Maintained in an Atherosclerotic Zbtb46-DTR Mouse Model. PLoS ONE. 2017;12:e0169608.
Not in our library10.1371/journal.pone.0169608
301.
McKenna H.J., Stocking K.L., Miller R.E., Brasel K., De Smedt T., Maraskovsky E., Maliszewski C.R., Lynch D.H., Smith J., Pulendran B., et al. Mice lacking flt3 ligand have deficient hematopoiesis affecting hematopoietic progenitor cells, dendritic cells, and natural killer cells. Blood. 2000;95:3489-3497.
Not in our library10.1182/blood.v95.11.3489
302.
Legein B., Janssen E.M., Theelen T.L., Gijbels M.J., Walraven J., Klarquist J.S., Hennies C.M., Wouters K., Seijkens T.T., Wijnands E., et al. Ablation of CD8alpha(+) dendritic cell mediated cross-presentation does not impact atherosclerosis in hyperlipidemic mice. Sci Rep. 2015;5:15414.
Not in our library10.1038/srep15414
303.
Gil-Pulido J., Cochain C., Lippert M.A., Schneider N., Butt E., Amezaga N., Zernecke A. Deletion of Batf3-dependent antigen-presenting cells does not affect atherosclerotic lesion formation in mice. PLoS ONE. 2017;12:e0181947.
Not in our library10.1371/journal.pone.0181947
304.
Li Y., Liu X., Duan W., Tian H., Zhu G., He H., Yao S., Yi S., Song W., Tang H. Batf3-dependent CD8alpha(+) Dendritic Cells Aggravates Atherosclerosis via Th1 Cell Induction and Enhanced CCL5 Expression in Plaque Macrophages. EBioMedicine. 2017;18:188-198.
Not in our library10.1016/j.ebiom.2017.04.008
305.
Haddad Y., Lahoute C., Clement M., Laurans L., Metghalchi S., Zeboudj L., Giraud A., Loyer X., Vandestienne M., Wain-Hobson J., et al. The Dendritic Cell Receptor DNGR-1 Promotes the Development of Atherosclerosis in Mice. Circ. Res. 2017;121:234-243.
Not in our library10.1161/circresaha.117.310960
306.
Daissormont I.T., Christ A., Temmerman L., Sampedro Millares S., Seijkens T., Manca M., Rousch M., Poggi M., Boon L., van der Loos C., et al. Plasmacytoid dendritic cells protect against atherosclerosis by tuning T-cell proliferation and activity. Circ. Res. 2011;109:1387-1395.
Not in our library10.1161/circresaha.111.256529
307.
Doring Y., Manthey H.D., Drechsler M., Lievens D., Megens R.T., Soehnlein O., Busch M., Manca M., Koenen R.R., Pelisek J., et al. Auto-antigenic protein-DNA complexes stimulate plasmacytoid dendritic cells to promote atherosclerosis. Circulation. 2012;125:1673-1683.
Not in our library10.1161/circulationaha.111.046755
308.
Macritchie N., Grassia G., Sabir S.R., Maddaluno M., Welsh P., Sattar N., Ialenti A., Kurowska-Stolarska M., McInnes I.B., Brewer J.M., et al. Plasmacytoid dendritic cells play a key role in promoting atherosclerosis in apolipoprotein E-deficient mice. Arterioscler. Thromb. Vasc. Biol. 2012;32:2569-2579.
Not in our library10.1161/atvbaha.112.251314
309.
Yun T.J., Lee J.S., Machmach K., Shim D., Choi J., Wi Y.J., Jang H.S., Jung I.H., Kim K., Yoon W.K., et al. Indoleamine 2,3-Dioxygenase-Expressing Aortic Plasmacytoid Dendritic Cells Protect against Atherosclerosis by Induction of Regulatory T Cells. Cell Metab. 2016;23:852-866.
Not in our library10.1016/j.cmet.2016.04.010
310.
Mandl M., Drechsler M., Jansen Y., Neideck C., Noels H., Faussner A., Soehnlein O., Weber C., Doring Y. Evaluation of the BDCA2-DTR Transgenic Mouse Model in Chronic and Acute Inflammation. PLoS ONE. 2015;10:e0134176.
Not in our library10.1371/journal.pone.0134176
311.
Sage A.P., Murphy D., Maffia P., Masters L.M., Sabir S.R., Baker L.L., Cambrook H., Finigan A.J., Ait-Oufella H., Grassia G., et al. MHC Class II-restricted antigen presentation by plasmacytoid dendritic cells drives proatherogenic T cell immunity. Circulation. 2014;130:1363-1373.
Not in our library10.1161/circulationaha.114.011090
312.
Kretzschmar D., Rohm I., Schaller S., Betge S., Pistulli R., Atiskova Y., Figulla H.R., Yilmaz A. Decrease in circulating dendritic cell precursors in patients with peripheral artery disease. Mediat. Inflamm. 2015;2015:450957.
Not in our library10.1155/2015/450957
313.
Van Vre E.A., Van Brussel I., Bosmans J.M., Vrints C.J., Bult H. Dendritic cells in human atherosclerosis: From circulation to atherosclerotic plaques. Mediat. Inflamm. 2011;2011:941396.
Not in our library10.1155/2011/941396
314.
Liu A., Ming J.Y., Fiskesund R., Ninio E., Karabina S.A., Bergmark C., Frostegard A.G., Frostegard J. Induction of dendritic cell-mediated T-cell activation by modified but not native low-density lipoprotein in humans and inhibition by annexin a5: Involvement of heat shock proteins. Arterioscler. Thromb. Vasc. Biol. 2015;35:197-205.
Not in our library10.1161/atvbaha.114.304342
315.
Fehervari Z., Sakaguchi S. Control of Foxp3+ CD25+CD4+ regulatory cell activation and function by dendritic cells. Int. Immunol. 2004;16:1769-1780.
Not in our library10.1093/intimm/dxh178
316.
Liu J., Cao X. Regulatory dendritic cells in autoimmunity: A comprehensive review. J. Autoimmun. 2015;63:1-12.
Not in our library10.1016/j.jaut.2015.07.011
317.
Morelli A.E., Thomson A.W. Tolerogenic dendritic cells and the quest for transplant tolerance. Nat. Rev. Immunol. 2007;7:610-621.
Not in our library10.1038/nri2132
318.
Chen M., Wang Y.H., Wang Y., Huang L., Sandoval H., Liu Y.J., Wang J. Dendritic cell apoptosis in the maintenance of immune tolerance. Science. 2006;311:1160-1164.
Not in our library10.1126/science.1122545
319.
Selenko-Gebauer N., Majdic O., Szekeres A., Hofler G., Guthann E., Korthauer U., Zlabinger G., Steinberger P., Pickl W.F., Stockinger H., et al. B7-H1 (programmed death-1 ligand) on dendritic cells is involved in the induction and maintenance of T cell anergy. J. Immunol. 2003;170:3637-3644.
Not in our library10.4049/jimmunol.170.7.3637
320.
Darrasse-Jeze G., Deroubaix S., Mouquet H., Victora G.D., Eisenreich T., Yao K.H., Masilamani R.F., Dustin M.L., Rudensky A., Liu K., et al. Feedback control of regulatory T cell homeostasis by dendritic cells in vivo. J. Exp. Med. 2009;206:1853-1862.
Not in our library10.1084/jem.20090746
321.
Selectins modify dendritic cells during atherosclerosis · 2018
Not checked
322.
Torres-Aguilar H., Sanchez-Torres C., Jara L.J., Blank M., Shoenfeld Y. IL-10/TGF-beta-treated dendritic cells, pulsed with insulin, specifically reduce the response to insulin of CD4+ effector/memory T cells from type 1 diabetic individuals. J. Clin. Immunol. 2010;30:659-668.
Not in our library10.1007/s10875-010-9430-5
323.
Hjerpe C., Johansson D., Hermansson A., Hansson G.K., Zhou X. Dendritic cells pulsed with malondialdehyde modified low density lipoprotein aggravate atherosclerosis in Apoe(-/-) mice. Atherosclerosis. 2010;209:436-441.
Not in our library10.1016/j.atherosclerosis.2009.10.003
324.
Frodermann V., van Puijvelde G.H., Wierts L., Lagraauw H.M., Foks A.C., van Santbrink P.J., Bot I., Kuiper J., de Jager S.C. Oxidized low-density lipoprotein-induced apoptotic dendritic cells as a novel therapy for atherosclerosis. J. Immunol. 2015;194:2208-2218.
Not in our library10.4049/jimmunol.1401843
325.
Ketelhuth D.F., Hansson G.K. Adaptive Response of T and B Cells in Atherosclerosis. Circ. Res. 2016;118:668-678.
Not in our library10.1161/circresaha.115.306427
326.
Bustos-Moran E., Blas-Rus N., Martin-Cofreces N.B., Sanchez-Madrid F. Orchestrating Lymphocyte Polarity in Cognate Immune Cell-Cell Interactions. Int. Rev. Cell Mol. Biol. 2016;327:195-261.
Not in our library10.1016/bs.ircmb.2016.06.004
327.
Gronberg C., Nilsson J., Wigren M. Recent advances on CD4(+) T cells in atherosclerosis and its implications for therapy. Eur. J. Pharmacol. 2017;816:58-66.
Not in our library10.1016/j.ejphar.2017.04.029
328.
Kaech S.M., Wherry E.J., Ahmed R. Effector and memory T-cell differentiation: Implications for vaccine development. Nat. Rev. Immunol. 2002;2:251-262.
Not in our library10.1038/nri778
329.
Zhou L., Chong M.M., Littman D.R. Plasticity of CD4+ T cell lineage differentiation. Immunity. 2009;30:646-655.
Not in our library10.1016/j.immuni.2009.05.001
330.
Rocha-Perugini V., Gonzalez-Granado J.M. Nuclear envelope lamin-A as a coordinator of T cell activation. Nucleus. 2014;5:396-401.
Not in our library10.4161/nucl.36361
331.
van Panhuys N., Klauschen F., Germain R.N. T-cell-receptor-dependent signal intensity dominantly controls CD4(+) T cell polarization In Vivo. Immunity. 2014;41:63-74.
Not in our library10.1016/j.immuni.2014.06.003
332.
Zhu J., Yamane H., Paul W.E. Differentiation of effector CD4 T cell populations (*). Annu. Rev. Immunol. 2010;28:445-489.
Not in our library10.1146/annurev-immunol-030409-101212
333.
Tse K., Tse H., Sidney J., Sette A., Ley K. T cells in atherosclerosis. Int. Immunol. 2013;25:615-622.
Not in our library10.1093/intimm/dxt043
334.
Zhu J., Paul W.E. CD4 T cells: Fates, functions, and faults. Blood. 2008;112:1557-1569.
Not in our library10.1182/blood-2008-05-078154
335.
Gounopoulos P., Merki E., Hansen L.F., Choi S.H., Tsimikas S. Antibodies to oxidized low density lipoprotein: Epidemiological studies and potential clinical applications in cardiovascular disease. Minerva Cardioangiol. 2007;55:821-837.
Not in our library
336.
Libby P. Inflammation in atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 2012;32:2045-2051.
Not in our library10.1161/atvbaha.108.179705
337.
Lahoute C., Herbin O., Mallat Z., Tedgui A. Adaptive immunity in atherosclerosis: Mechanisms and future therapeutic targets. Nat. Rev. Cardiol. 2011;8:348-358.
Not in our library10.1038/nrcardio.2011.62
338.
Iborra S., Gonzalez-Granado J.M. In Vitro Differentiation of Naive CD4(+) T Cells: A Tool for Understanding the Development of Atherosclerosis. Methods Mol. Biol. 2015;1339:177-189.
Not in our library10.1007/978-1-4939-2929-0_12
339.
Aubry M.C., Riehle D.L., Edwards W.D., Maradit-Kremers H., Roger V.L., Sebo T.J., Gabriel S.E. B-Lymphocytes in plaque and adventitia of coronary arteries in two patients with rheumatoid arthritis and coronary atherosclerosis: Preliminary observations. Cardiovasc. Pathol. 2004;13:233-236.
Not in our library10.1016/j.carpath.2004.02.005
340.
Ketelhuth D.F., Hansson G.K. Cellular immunity, low-density lipoprotein and atherosclerosis: Break of tolerance in the artery wall. Thromb. Haemost. 2011;106:779-786.
Not in our library10.1160/th11-05-0321
341.
Mallat Z., Taleb S., Ait-Oufella H., Tedgui A. The role of adaptive T cell immunity in atherosclerosis. J. Lipid Res. 2009;50(Suppl.):S364-S369.
Not in our library10.1194/jlr.r800092-jlr200
342.
Laurat E., Poirier B., Tupin E., Caligiuri G., Hansson G.K., Bariety J., Nicoletti A. In vivo downregulation of T helper cell 1 immune responses reduces atherogenesis in apolipoprotein E-knockout mice. Circulation. 2001;104:197-202.
Not in our library10.1161/01.cir.104.2.197
343.
Li J., McArdle S., Gholami A., Kimura T., Wolf D., Gerhardt T., Miller J., Weber C., Ley K. CCR5+T-bet+FoxP3+ Effector CD4 T Cells Drive Atherosclerosis. Circ. Res. 2016;118:1540-1552.
Not in our library10.1161/circresaha.116.308648
344.
Elhage R., Gourdy P., Brouchet L., Jawien J., Fouque M.J., Fievet C., Huc X., Barreira Y., Couloumiers J.C., Arnal J.F., et al. Deleting TCR alpha beta+ or CD4+ T lymphocytes leads to opposite effects on site-specific atherosclerosis in female apolipoprotein E-deficient mice. Am. J. Pathol. 2004;165:2013-2018.
Not in our library10.1016/s0002-9440(10)63252-x
345.
Zhou X., Robertson A.K., Rudling M., Parini P., Hansson G.K. Lesion development and response to immunization reveal a complex role for CD4 in atherosclerosis. Circ. Res. 2005;96:427-434.
Not in our library10.1161/01.res.0000156889.22364.f1
346.
Buono C., Binder C.J., Stavrakis G., Witztum J.L., Glimcher L.H., Lichtman A.H. T-bet deficiency reduces atherosclerosis and alters plaque antigen-specific immune responses. Proc. Natl. Acad. Sci. USA. 2005;102:1596-1601.
Not in our library10.1073/pnas.0409015102
347.
Buono C., Come C.E., Stavrakis G., Maguire G.F., Connelly P.W., Lichtman A.H. Influence of interferon-gamma on the extent and phenotype of diet-induced atherosclerosis in the LDLR-deficient mouse. Arterioscler. Thromb. Vasc. Biol. 2003;23:454-460.
Not in our library10.1161/01.atv.0000059419.11002.6e
348.
Jones K.L., Maguire J.J., Davenport A.P. Chemokine receptor CCR5: From AIDS to atherosclerosis. Br. J. Pharmacol. 2011;162:1453-1469.
Not in our library10.1111/j.1476-5381.2010.01147.x
349.
Elhage R., Jawien J., Rudling M., Ljunggren H.G., Takeda K., Akira S., Bayard F., Hansson G.K. Reduced atherosclerosis in interleukin-18 deficient apolipoprotein E-knockout mice. Cardiovasc. Res. 2003;59:234-240.
Not in our library10.1016/s0008-6363(03)00343-2
350.
Davenport P., Tipping P.G. The role of interleukin-4 and interleukin-12 in the progression of atherosclerosis in apolipoprotein E-deficient mice. Am. J. Pathol. 2003;163:1117-1125.
Not in our library10.1016/s0002-9440(10)63471-2
351.
Hauer A.D., Uyttenhove C., de Vos P., Stroobant V., Renauld J.C., van Berkel T.J., van Snick J., Kuiper J. Blockade of interleukin-12 function by protein vaccination attenuates atherosclerosis. Circulation. 2005;112:1054-1062.
Not in our library10.1161/circulationaha.104.533463
352.
Mallat Z., Corbaz A., Scoazec A., Graber P., Alouani S., Esposito B., Humbert Y., Chvatchko Y., Tedgui A. Interleukin-18/interleukin-18 binding protein signaling modulates atherosclerotic lesion development and stability. Circ. Res. 2001;89:E41-E45.
Not in our library10.1161/hh1901.098735
353.
Haybar H., Rezaeeyan H., Shahjahani M., Shirzad R., Saki N. T-bet transcription factor in cardiovascular disease: Attenuation or inflammation factor? J. Cell. Physiol. 2019;234:7915-7922.
Not in our library10.1002/jcp.27935
354.
Oh S., Hwang E.S. The role of protein modifications of T-bet in cytokine production and differentiation of T helper cells. J. Immunol. Res. 2014;2014:589672.
Not in our library10.1155/2014/589672
355.
Yu F., Sharma S., Edwards J., Feigenbaum L., Zhu J. Dynamic expression of transcription factors T-bet and GATA-3 by regulatory T cells maintains immunotolerance. Nat. Immunol. 2015;16:197-206.
Not in our library10.1038/ni.3053
356.
Whitman S.C., Ravisankar P., Elam H., Daugherty A. Exogenous interferon-gamma enhances atherosclerosis in apolipoprotein E-/- mice. Am. J. Pathol. 2000;157:1819-1824.
Not in our library10.1016/s0002-9440(10)64820-1
357.
Gupta S., Pablo A.M., Jiang X., Wang N., Tall A.R., Schindler C. IFN-gamma potentiates atherosclerosis in ApoE knock-out mice. J. Clin. Investig. 1997;99:2752-2761.
Not in our library10.1172/jci119465
358.
Moss J.W., Ramji D.P. Interferon-gamma: Promising therapeutic target in atherosclerosis. World J. Exp. Med. 2015;5:154-159.
Not in our library10.5493/wjem.v5.i3.154
359.
Lim W.S., Timmins J.M., Seimon T.A., Sadler A., Kolodgie F.D., Virmani R., Tabas I. Signal transducer and activator of transcription-1 is critical for apoptosis in macrophages subjected to endoplasmic reticulum stress in vitro and in advanced atherosclerotic lesions in vivo. Circulation. 2008;117:940-951.
Not in our library10.1161/circulationaha.107.711275
360.
Blankenberg S., Barbaux S., Tiret L. Adhesion molecules and atherosclerosis. Atherosclerosis. 2003;170:191-203.
Not in our library10.1016/s0021-9150(03)00097-2
361.
Chung H.K., Lee I.K., Kang H., Suh J.M., Kim H., Park K.C., Kim D.W., Kim Y.K., Ro H.K., Shong M. Statin inhibits interferon-gamma-induced expression of intercellular adhesion molecule-1 (ICAM-1) in vascular endothelial and smooth muscle cells. Exp. Mol. Med. 2002;34:451-461.
Not in our library10.1038/emm.2002.63
362.
Harvey E.J., Ramji D.P. Interferon-gamma and atherosclerosis: Pro- or anti-atherogenic? Cardiovasc. Res. 2005;67:11-20.
Not in our library10.1016/j.cardiores.2005.04.019
363.
Canton J., Neculai D., Grinstein S. Scavenger receptors in homeostasis and immunity. Nat. Rev. Immunol. 2013;13:621-634.
Not in our library10.1038/nri3515
364.
Kzhyshkowska J., Neyen C., Gordon S. Role of macrophage scavenger receptors in atherosclerosis. Immunobiology. 2012;217:492-502.
Not in our library10.1016/j.imbio.2012.02.015
365.
Wuttge D.M., Zhou X., Sheikine Y., Wagsater D., Stemme V., Hedin U., Stemme S., Hansson G.K., Sirsjo A. CXCL16/SR-PSOX is an interferon-gamma-regulated chemokine and scavenger receptor expressed in atherosclerotic lesions. Arterioscler. Thromb. Vasc. Biol. 2004;24:750-755.
Not in our library10.1161/01.atv.0000124102.11472.36
366.
Braunersreuther V., Zernecke A., Arnaud C., Liehn E.A., Steffens S., Shagdarsuren E., Bidzhekov K., Burger F., Pelli G., Luckow B., et al. Ccr5 but not Ccr1 deficiency reduces development of diet-induced atherosclerosis in mice. Arterioscler. Thromb. Vasc. Biol. 2007;27:373-379.
Not in our library10.1161/01.atv.0000253886.44609.ae
367.
Afzal A.R., Kiechl S., Daryani Y.P., Weerasinghe A., Zhang Y., Reindl M., Mayr A., Weger S., Xu Q., Willeit J. Common CCR5-del32 frameshift mutation associated with serum levels of inflammatory markers and cardiovascular disease risk in the Bruneck population. Stroke. 2008;39:1972-1978.
Not in our library10.1161/strokeaha.107.504381
368.
Szalai C., Duba J., Prohaszka Z., Kalina A., Szabo T., Nagy B., Horvath L., Csaszar A. Involvement of polymorphisms in the chemokine system in the susceptibility for coronary artery disease (CAD). Coincidence of elevated Lp(a) and MCP-1 -2518 G/G genotype in CAD patients. Atherosclerosis. 2001;158:233-239.
Not in our library10.1016/s0021-9150(01)00423-3
369.
Pai J.K., Kraft P., Cannuscio C.C., Manson J.E., Rexrode K.M., Albert C.M., Hunter D., Rimm E.B. Polymorphisms in the CC-chemokine receptor-2 (CCR2) and -5 (CCR5) genes and risk of coronary heart disease among US women. Atherosclerosis. 2006;186:132-139.
Not in our library10.1016/j.atherosclerosis.2005.06.041
370.
Balistreri C.R., Candore G., Caruso M., Incalcaterra E., Franceschi C., Caruso C. Role of polymorphisms of CC-chemokine receptor-5 gene in acute myocardial infarction and biological implications for longevity. Haematologica. 2008;93:637-638.
Not in our library10.3324/haematol.12239
371.
Gonzalez P., Alvarez R., Batalla A., Reguero J.R., Alvarez V., Astudillo A., Cubero G.I., Cortina A., Coto E. Genetic variation at the chemokine receptors CCR5/CCR2 in myocardial infarction. Genes Immun. 2001;2:191-195.
Not in our library10.1038/sj.gene.6363760
372.
Sharda S., Gilmour A., Harris V., Singh V.P., Sinha N., Tewari S., Ramesh V., Agrawal S., Mastana S. Chemokine receptor 5 (CCR5) deletion polymorphism in North Indian patients with coronary artery disease. Int. J. Cardiol. 2008;124:254-258.
Not in our library10.1016/j.ijcard.2006.12.021
373.
Ghilardi G., Biondi M.L., Turri O., Pateri F., d’Eril G.M., Scorza R. Genetic control of chemokines in severe human internal carotid artery stenosis. Cytokine. 2008;41:24-28.
Not in our library10.1016/j.cyto.2007.10.007
374.
Apostolakis S., Baritaki S., Kochiadakis G.E., Igoumenidis N.E., Panutsopulos D., Spandidos D.A. Effects of polymorphisms in chemokine ligands and receptors on susceptibility to coronary artery disease. Thromb Res. 2007;119:63-71.
Not in our library10.1016/j.thromres.2005.12.016
375.
Petrkova J., Cermakova Z., Lukl J., Petrek M. CC chemokine receptor 5 (CCR5) deletion polymorphism does not protect Czech males against early myocardial infarction. J. Intern. Med. 2005;257:564-566.
Not in our library10.1111/j.1365-2796.2005.01491.x
376.
Simeoni E., Winkelmann B.R., Hoffmann M.M., Fleury S., Ruiz J., Kappenberger L., Marz W., Vassalli G. Association of RANTES G-403A gene polymorphism with increased risk of coronary arteriosclerosis. Eur. Heart J. 2004;25:1438-1446.
Not in our library10.1016/j.ehj.2004.05.005
377.
van Wanrooij E.J., Happe H., Hauer A.D., de Vos P., Imanishi T., Fujiwara H., van Berkel T.J., Kuiper J. HIV entry inhibitor TAK-779 attenuates atherogenesis in low-density lipoprotein receptor-deficient mice. Arterioscler. Thromb. Vasc. Biol. 2005;25:2642-2647.
Not in our library10.1161/01.atv.0000192018.90021.c0
378.
Veillard N.R., Kwak B., Pelli G., Mulhaupt F., James R.W., Proudfoot A.E., Mach F. Antagonism of RANTES receptors reduces atherosclerotic plaque formation in mice. Circ. Res. 2004;94:253-261.
Not in our library10.1161/01.res.0000109793.17591.4e
379.
Schober A., Manka D., von Hundelshausen P., Huo Y., Hanrath P., Sarembock I.J., Ley K., Weber C. Deposition of platelet RANTES triggering monocyte recruitment requires P-selectin and is involved in neointima formation after arterial injury. Circulation. 2002;106:1523-1529.
Not in our library10.1161/01.cir.0000028590.02477.6f
380.
Quinones M.P., Martinez H.G., Jimenez F., Estrada C.A., Dudley M., Willmon O., Kulkarni H., Reddick R.L., Fernandes G., Kuziel W.A., et al. CC chemokine receptor 5 influences late-stage atherosclerosis. Atherosclerosis. 2007;195:e92-e103.
Not in our library10.1016/j.atherosclerosis.2007.03.026
381.
Potteaux S., Combadiere C., Esposito B., Lecureuil C., Ait-Oufella H., Merval R., Ardouin P., Tedgui A., Mallat Z. Role of bone marrow-derived CC-chemokine receptor 5 in the development of atherosclerosis of low-density lipoprotein receptor knockout mice. Arterioscler. Thromb. Vasc. Biol. 2006;26:1858-1863.
Not in our library10.1161/01.atv.0000231527.22762.71
382.
Luckow B., Joergensen J., Chilla S., Li J.P., Henger A., Kiss E., Wieczorek G., Roth L., Hartmann N., Hoffmann R., et al. Reduced intragraft mRNA expression of matrix metalloproteinases Mmp3, Mmp12, Mmp13 and Adam8, and diminished transplant arteriosclerosis in Ccr5-deficient mice. Eur. J. Immunol. 2004;34:2568-2578.
Not in our library10.1002/eji.200324776
383.
Kuziel W.A., Dawson T.C., Quinones M., Garavito E., Chenaux G., Ahuja S.S., Reddick R.L., Maeda N. CCR5 deficiency is not protective in the early stages of atherogenesis in apoE knockout mice. Atherosclerosis. 2003;167:25-32.
Not in our library10.1016/s0021-9150(02)00382-9
384.
Piconi S., Pocaterra D., Rainone V., Cossu M., Masetti M., Rizzardini G., Clerici M., Trabattoni D. Maraviroc Reduces Arterial Stiffness in PI-Treated HIV-infected Patients. Sci. Rep. 2016;6:28853.
Not in our library10.1038/srep28853
385.
Cipriani S., Francisci D., Mencarelli A., Renga B., Schiaroli E., D’Amore C., Baldelli F., Fiorucci S. Efficacy of the CCR5 antagonist maraviroc in reducing early, ritonavir-induced atherogenesis and advanced plaque progression in mice. Circulation. 2013;127:2114-2124.
Not in our library10.1161/circulationaha.113.001278
386.
Krohn R., Raffetseder U., Bot I., Zernecke A., Shagdarsuren E., Liehn E.A., van Santbrink P.J., Nelson P.J., Biessen E.A., Mertens P.R., et al. Y-box binding protein-1 controls CC chemokine ligand-5 (CCL5) expression in smooth muscle cells and contributes to neointima formation in atherosclerosis-prone mice. Circulation. 2007;116:1812-1820.
Not in our library10.1161/circulationaha.107.708016
387.
Braunersreuther V., Steffens S., Arnaud C., Pelli G., Burger F., Proudfoot A., Mach F. A novel RANTES antagonist prevents progression of established atherosclerotic lesions in mice. Arterioscler. Thromb. Vasc. Biol. 2008;28:1090-1096.
Not in our library10.1161/atvbaha.108.165423
388.
Robertson A.K., Rudling M., Zhou X., Gorelik L., Flavell R.A., Hansson G.K. Disruption of TGF-beta signaling in T cells accelerates atherosclerosis. J. Clin. Investig. 2003;112:1342-1350.
Not in our library10.1172/jci18607
389.
Ho I.C., Tai T.S., Pai S.Y. GATA3 and the T-cell lineage: Essential functions before and after T-helper-2-cell differentiation. Nat. Rev. Immunol. 2009;9:125-135.
Not in our library10.1038/nri2476
390.
Engelbertsen D., Andersson L., Ljungcrantz I., Wigren M., Hedblad B., Nilsson J., Bjorkbacka H. T-helper 2 immunity is associated with reduced risk of myocardial infarction and stroke. Arterioscler. Thromb. Vasc. Biol. 2013;33:637-644.
Not in our library10.1161/atvbaha.112.300871
391.
Mantani P.T., Duner P., Bengtsson E., Alm R., Ljungcrantz I., Soderberg I., Sundius L., To F., Nilsson J., Bjorkbacka H., et al. IL-25 inhibits atherosclerosis development in apolipoprotein E deficient mice. PLoS ONE. 2015;10:e0117255.
Not in our library10.1371/journal.pone.0117255
392.
Silveira A., McLeod O., Strawbridge R.J., Gertow K., Sennblad B., Baldassarre D., Veglia F., Deleskog A., Persson J., Leander K., et al. Plasma IL-5 concentration and subclinical carotid atherosclerosis. Atherosclerosis. 2015;239:125-130.
Not in our library10.1016/j.atherosclerosis.2014.12.046
393.
Binder C.J., Hartvigsen K., Chang M.K., Miller M., Broide D., Palinski W., Curtiss L.K., Corr M., Witztum J.L. IL-5 links adaptive and natural immunity specific for epitopes of oxidized LDL and protects from atherosclerosis. J. Clin. Investig. 2004;114:427-437.
Not in our library10.1172/jci200420479
394.
Interleukin‐13 protects from atherosclerosis and modulates plaque composition by skewing the macrophage phenotype · 2012
No notice
395.
Engelbertsen D., Rattik S., Knutsson A., Bjorkbacka H., Bengtsson E., Nilsson J. Induction of T helper 2 responses against human apolipoprotein B100 does not affect atherosclerosis in ApoE-/- mice. Cardiovasc. Res. 2014;103:304-312.
Not in our library10.1093/cvr/cvu131
396.
King V.L., Szilvassy S.J., Daugherty A. Interleukin-4 deficiency decreases atherosclerotic lesion formation in a site-specific manner in female LDL receptor-/- mice. Arterioscler. Thromb. Vasc. Biol. 2002;22:456-461.
Not in our library10.1161/hq0302.104905
397.
King V.L., Cassis L.A., Daugherty A. Interleukin-4 does not influence development of hypercholesterolemia or angiotensin II-induced atherosclerotic lesions in mice. Am. J. Pathol. 2007;171:2040-2047.
Not in our library10.2353/ajpath.2007.060857
398.
Huang J.T., Welch J.S., Ricote M., Binder C.J., Willson T.M., Kelly C., Witztum J.L., Funk C.D., Conrad D., Glass C.K. Interleukin-4-dependent production of PPAR-gamma ligands in macrophages by 12/15-lipoxygenase. Nature. 1999;400:378-382.
Not in our library10.1038/22572
399.
Cornicelli J.A., Butteiger D., Rateri D.L., Welch K., Daugherty A. Interleukin-4 augments acetylated LDL-induced cholesterol esterification in macrophages. J. Lipid Res. 2000;41:376-383.
Not in our library
400.
Barks J.L., McQuillan J.J., Iademarco M.F. TNF-alpha and IL-4 synergistically increase vascular cell adhesion molecule-1 expression in cultured vascular smooth muscle cells. J. Immunol. 1997;159:4532-4538.
Not in our library
401.
Lee Y.W., Kuhn H., Hennig B., Neish A.S., Toborek M. IL-4-induced oxidative stress upregulates VCAM-1 gene expression in human endothelial cells. J. Mol. Cell. Cardiol. 2001;33:83-94.
Not in our library10.1006/jmcc.2000.1278
402.
Sasaguri T., Arima N., Tanimoto A., Shimajiri S., Hamada T., Sasaguri Y. A role for interleukin 4 in production of matrix metalloproteinase 1 by human aortic smooth muscle cells. Atherosclerosis. 1998;138:247-253.
Not in our library10.1016/s0021-9150(97)00296-7
403.
Walch L., Massade L., Dufilho M., Brunet A., Rendu F. Pro-atherogenic effect of interleukin-4 in endothelial cells: Modulation of oxidative stress, nitric oxide and monocyte chemoattractant protein-1 expression. Atherosclerosis. 2006;187:285-291.
Not in our library10.1016/j.atherosclerosis.2005.09.016
404.
Vila-Caballer M., Gonzalez-Granado J.M., Zorita V., Abu Nabah Y.N., Silvestre-Roig C., Del Monte-Monge A., Molina-Sanchez P., Ait-Oufella H., Andres-Manzano M.J., Sanz M.J., et al. Disruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in mice. J. Mol. Cell. Cardiol. 2019;132:154-163.
Not in our library10.1016/j.yjmcc.2019.05.009
405.
Huang Y., Hu H., Liu L., Ye J., Wang Z., Que B., Liu W., Shi Y., Zeng T., Shi L., et al. Interleukin-12p35 Deficiency Reverses the Th1/Th2 Imbalance, Aggravates the Th17/Treg Imbalance, and Ameliorates Atherosclerosis in ApoE-/- Mice. Mediat. Inflamm. 2019;2019:3152040.
Not in our library10.1155/2019/3152040
406.
Gao S., Zhang W., Zhao Q., Zhou J., Wu Y., Liu Y., Yuan Z., Wang L. Curcumin ameliorates atherosclerosis in apolipoprotein E deficient asthmatic mice by regulating the balance of Th2/Treg cells. Phytomedicine. 2019;52:129-135.
Not in our library10.1016/j.phymed.2018.09.194
407.
Gaffen S.L. Structure and signalling in the IL-17 receptor family. Nat. Rev. Immunol. 2009;9:556-567.
Not in our library10.1038/nri2586
408.
Selmi C. Autoimmunity in 2018. Clin. Rev. Allergy Immunol. 2019;56:375-384.
Not in our library10.1007/s12016-019-08745-w
409.
Akhavanpoor M., Akhavanpoor H., Gleissner C.A., Wangler S., Doesch A.O., Katus H.A., Erbel C. The Two Faces of Interleukin-17A in Atherosclerosis. Curr. Drug Targets. 2017;18:863-873.
Not in our library10.2174/1389450117666161229142155
410.
Allam G., Abdel-Moneim A., Gaber A.M. The pleiotropic role of interleukin-17 in atherosclerosis. Biomed. Pharmacother. 2018;106:1412-1418.
Not in our library10.1016/j.biopha.2018.07.110
411.
Lu X. The Impact of IL-17 in Atherosclerosis. Curr. Med. Chem. 2017;24:2345-2358.
Not in our library10.2174/0929867324666170419150614
412.
Zheng Y., Li T. Interleukin-22, a potent target for treatment of non-autoimmune diseases. Hum. Vaccin. Immunother. 2018;14:2811-2819.
Not in our library10.1080/21645515.2018.1509649
413.
Taleb S., Tedgui A. IL-17 in atherosclerosis: The good and the bad. Cardiovasc. Res. 2018;114:7-9.
Not in our library10.1093/cvr/cvx225
414.
Smith E., Prasad K.M., Butcher M., Dobrian A., Kolls J.K., Ley K., Galkina E. Blockade of interleukin-17A results in reduced atherosclerosis in apolipoprotein E-deficient mice. Circulation. 2010;121:1746-1755.
Not in our library10.1161/circulationaha.109.924886
415.
El-Behi M., Ciric B., Dai H., Yan Y., Cullimore M., Safavi F., Zhang G.X., Dittel B.N., Rostami A. The encephalitogenicity of T(H)17 cells is dependent on IL-1- and IL-23-induced production of the cytokine GM-CSF. Nat. Immunol. 2011;12:568-575.
Not in our library10.1038/ni.2031
416.
Ogura H., Murakami M., Okuyama Y., Tsuruoka M., Kitabayashi C., Kanamoto M., Nishihara M., Iwakura Y., Hirano T. Interleukin-17 promotes autoimmunity by triggering a positive-feedback loop via interleukin-6 induction. Immunity. 2008;29:628-636.
Not in our library10.1016/j.immuni.2008.07.018
417.
Weaver C.T., Hatton R.D. Interplay between the TH17 and TReg cell lineages: A (co-)evolutionary perspective. Nat. Rev. Immunol. 2009;9:883-889.
Not in our library10.1038/nri2660
418.
Zuniga L.A., Jain R., Haines C., Cua D.J. Th17 cell development: From the cradle to the grave. Immunol. Rev. 2013;252:78-88.
Not in our library10.1111/imr.12036
419.
T-bet is a key modulator of IL-23-driven pathogenic CD4+ T cell responses in the intestine · 2016
Not checked
420.
Abdel-Moneim A., Bakery H.H., Allam G. The potential pathogenic role of IL-17/Th17 cells in both type 1 and type 2 diabetes mellitus. Biomed. Pharmacother. 2018;101:287-292.
Not in our library10.1016/j.biopha.2018.02.103
421.
Hirota K., Duarte J.H., Veldhoen M., Hornsby E., Li Y., Cua D.J., Ahlfors H., Wilhelm C., Tolaini M., Menzel U., et al. Fate mapping of IL-17-producing T cells in inflammatory responses. Nat. Immunol. 2011;12:255-263.
Not in our library10.1038/ni.1993
422.
Lee Y., Awasthi A., Yosef N., Quintana F.J., Xiao S., Peters A., Wu C., Kleinewietfeld M., Kunder S., Hafler D.A., et al. Induction and molecular signature of pathogenic TH17 cells. Nat. Immunol. 2012;13:991-999.
Not in our library10.1038/ni.2416
423.
Gagliani N., Amezcua Vesely M.C., Iseppon A., Brockmann L., Xu H., Palm N.W., de Zoete M.R., Licona-Limon P., Paiva R.S., Ching T., et al. Th17 cells transdifferentiate into regulatory T cells during resolution of inflammation. Nature. 2015;523:221-225.
Not in our library10.1038/nature14452
424.
Korn T., Bettelli E., Oukka M., Kuchroo V.K. IL-17 and Th17 Cells. Annu Rev. Immunol. 2009;27:485-517.
Not in our library10.1146/annurev.immunol.021908.132710
425.
Liuzzo G., Trotta F., Pedicino D. Interleukin-17 in atherosclerosis and cardiovascular disease: The good, the bad, and the unknown. Eur. Heart J. 2013;34:556-559.
Not in our library10.1093/eurheartj/ehs399
426.
Yao Z., Painter S.L., Fanslow W.C., Ulrich D., Macduff B.M., Spriggs M.K., Armitage R.J. Human IL-17: A novel cytokine derived from T cells. J. Immunol. 1995;155:5483-5486.
Not in our library
427.
Harrington L.E., Hatton R.D., Mangan P.R., Turner H., Murphy T.L., Murphy K.M., Weaver C.T. Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nat. Immunol. 2005;6:1123-1132.
Not in our library10.1038/ni1254
428.
Butcher M., Galkina E. Current views on the functions of interleukin-17A-producing cells in atherosclerosis. Thromb. Haemost. 2011;106:787-795.
Not in our library10.1160/th11-05-0342
429.
Erbel C., Chen L., Bea F., Wangler S., Celik S., Lasitschka F., Wang Y., Bockler D., Katus H.A., Dengler T.J. Inhibition of IL-17A attenuates atherosclerotic lesion development in apoE-deficient mice. J. Immunol. 2009;183:8167-8175.
Not in our library10.4049/jimmunol.0901126
430.
Jovanovic D.V., Di Battista J.A., Martel-Pelletier J., Jolicoeur F.C., He Y., Zhang M., Mineau F., Pelletier J.P. IL-17 stimulates the production and expression of proinflammatory cytokines, IL-beta and TNF-alpha, by human macrophages. J. Immunol. 1998;160:3513-3521.
Not in our library
431.
Madhur M.S., Funt S.A., Li L., Vinh A., Chen W., Lob H.E., Iwakura Y., Blinder Y., Rahman A., Quyyumi A.A., et al. Role of interleukin 17 in inflammation, atherosclerosis, and vascular function in apolipoprotein e-deficient mice. Arterioscler. Thromb. Vasc. Biol. 2011;31:1565-1572.
Not in our library10.1161/atvbaha.111.227629
432.
Beringer A., Noack M., Miossec P. IL-17 in Chronic Inflammation: From Discovery to Targeting. Trends Mol. Med. 2016;22:230-241.
Not in our library10.1016/j.molmed.2016.01.001
433.
Ley K., Smith E., Stark M.A. IL-17A-producing neutrophil-regulatory Tn lymphocytes. Immunol. Res. 2006;34:229-242.
Not in our library10.1385/ir:34:3:229
434.
Taleb S., Romain M., Ramkhelawon B., Uyttenhove C., Pasterkamp G., Herbin O., Esposito B., Perez N., Yasukawa H., Van Snick J., et al. Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosis. J. Exp. Med. 2009;206:2067-2077.
Not in our library10.1084/jem.20090545
435.
Gistera A., Robertson A.K., Andersson J., Ketelhuth D.F., Ovchinnikova O., Nilsson S.K., Lundberg A.M., Li M.O., Flavell R.A., Hansson G.K. Transforming growth factor-beta signaling in T cells promotes stabilization of atherosclerotic plaques through an interleukin-17-dependent pathway. Sci. Transl. Med. 2013;5:196ra100.
Not in our library10.1126/scitranslmed.3006133
436.
Zhu F., Wang Q., Guo C., Wang X., Cao X., Shi Y., Gao F., Ma C., Zhang L. IL-17 induces apoptosis of vascular endothelial cells: A potential mechanism for human acute coronary syndrome. Clin. Immunol. 2011;141:152-160.
Not in our library10.1016/j.clim.2011.07.003
437.
Madhur M.S., Lob H.E., McCann L.A., Iwakura Y., Blinder Y., Guzik T.J., Harrison D.G. Interleukin 17 promotes angiotensin II-induced hypertension and vascular dysfunction. Hypertension. 2010;55:500-507.
Not in our library10.1161/hypertensionaha.109.145094
438.
Danzaki K., Matsui Y., Ikesue M., Ohta D., Ito K., Kanayama M., Kurotaki D., Morimoto J., Iwakura Y., Yagita H., et al. Interleukin-17A deficiency accelerates unstable atherosclerotic plaque formation in apolipoprotein E-deficient mice. Arterioscler. Thromb. Vasc. Biol. 2012;32:273-280.
Not in our library10.1161/atvbaha.111.229997
439.
van Es T., van Puijvelde G.H., Ramos O.H., Segers F.M., Joosten L.A., van den Berg W.B., Michon I.M., de Vos P., van Berkel T.J., Kuiper J. Attenuated atherosclerosis upon IL-17R signaling disruption in LDLr deficient mice. Biochem. Biophys. Res. Commun. 2009;388:261-265.
Not in our library10.1016/j.bbrc.2009.07.152
440.
Butcher M.J., Gjurich B.N., Phillips T., Galkina E.V. The IL-17A/IL-17RA axis plays a proatherogenic role via the regulation of aortic myeloid cell recruitment. Circ. Res. 2012;110:675-687.
Not in our library10.1161/circresaha.111.261784
441.
Gao Q., Jiang Y., Ma T., Zhu F., Gao F., Zhang P., Guo C., Wang Q., Wang X., Ma C., et al. A critical function of Th17 proinflammatory cells in the development of atherosclerotic plaque in mice. J. Immunol. 2010;185:5820-5827.
Not in our library10.4049/jimmunol.1000116
442.
Nordlohne J., von Vietinghoff S. Interleukin 17A in atherosclerosis - Regulation and pathophysiologic effector function. Cytokine. 2017;122:154089.
Not in our library10.1016/j.cyto.2017.06.016
443.
Butcher M.J., Waseem T.C., Galkina E.V. Smooth Muscle Cell-Derived Interleukin-17C Plays an Atherogenic Role via the Recruitment of Proinflammatory Interleukin-17A+ T Cells to the Aorta. Arterioscler. Thromb. Vasc. Biol. 2016;36:1496-1506.
Not in our library10.1161/atvbaha.116.307892
444.
Sedda S., Marafini I., Figliuzzi M.M., Pallone F., Monteleone G. An overview of the role of innate lymphoid cells in gut infections and inflammation. Mediat. Inflamm. 2014;2014:235460.
Not in our library10.1155/2014/235460
445.
Kumar P., Thakar M.S., Ouyang W., Malarkannan S. IL-22 from conventional NK cells is epithelial regenerative and inflammation protective during influenza infection. Mucosal Immunol. 2013;6:69-82.
Not in our library10.1038/mi.2012.49
446.
Regulation of TH17 Cells and Associated Cytokines in Wound Healing, Tissue Regeneration, and Carcinogenesis · 2017
No notice
447.
Zenewicz L.A., Yancopoulos G.D., Valenzuela D.M., Murphy A.J., Karow M., Flavell R.A. Interleukin-22 but not interleukin-17 provides protection to hepatocytes during acute liver inflammation. Immunity. 2007;27:647-659.
Not in our library10.1016/j.immuni.2007.07.023
448.
Gong F., Wu J., Zhou P., Zhang M., Liu J., Liu Y., Lu X., Liu Z. Interleukin-22 Might Act as a Double-Edged Sword in Type 2 Diabetes and Coronary Artery Disease. Mediat. Inflamm. 2016;2016:8254797.
Not in our library10.1155/2016/8254797
449.
Eyerich S., Eyerich K., Pennino D., Carbone T., Nasorri F., Pallotta S., Cianfarani F., Odorisio T., Traidl-Hoffmann C., Behrendt H., et al. Th22 cells represent a distinct human T cell subset involved in epidermal immunity and remodeling. J. Clin. Investig. 2009;119:3573-3585.
Not in our library10.1172/jci40202
450.
Ouyang W., Rutz S., Crellin N.K., Valdez P.A., Hymowitz S.G. Regulation and functions of the IL-10 family of cytokines in inflammation and disease. Annu. Rev. Immunol. 2011;29:71-109.
Not in our library10.1146/annurev-immunol-031210-101312
451.
Xia Q., Xiang X., Patel S., Puranik R., Xie Q., Bao S. Characterisation of IL-22 and interferon-gamma-inducible chemokines in human carotid plaque. Int. J. Cardiol. 2012;154:187-189.
Not in our library10.1016/j.ijcard.2011.10.093
452.
Chellan B., Yan L., Sontag T.J., Reardon C.A., Hofmann Bowman M.A. IL-22 is induced by S100/calgranulin and impairs cholesterol efflux in macrophages by downregulating ABCG1. J. Lipid Res. 2014;55:443-454.
Not in our library10.1194/jlr.m044305
453.
Rattik S., Hultman K., Rauch U., Soderberg I., Sundius L., Ljungcrantz I., Hultgardh-Nilsson A., Wigren M., Bjorkbacka H., Fredrikson G.N., et al. IL-22 affects smooth muscle cell phenotype and plaque formation in apolipoprotein E knockout mice. Atherosclerosis. 2015;242:506-514.
Not in our library10.1016/j.atherosclerosis.2015.08.006
454.
Fatkhullina A.R., Peshkova I.O., Dzutsev A., Aghayev T., McCulloch J.A., Thovarai V., Badger J.H., Vats R., Sundd P., Tang H.Y., et al. An Interleukin-23-Interleukin-22 Axis Regulates Intestinal Microbial Homeostasis to Protect from Diet-Induced Atherosclerosis. Immunity. 2018;49:943-957.
Not in our library10.1016/j.immuni.2018.09.011
455.
Sakaguchi S., Sakaguchi N., Asano M., Itoh M., Toda M. Immunologic self-tolerance maintained by activated T cells expressing IL-2 receptor alpha-chains (CD25). Breakdown of a single mechanism of self-tolerance causes various autoimmune diseases. J. Immunol. 1995;155:1151-1164.
Not in our library
456.
Apostolou I., von Boehmer H. In vivo instruction of suppressor commitment in naive T cells. J. Exp. Med. 2004;199:1401-1408.
Not in our library10.1084/jem.20040249
457.
Ray A., Khare A., Krishnamoorthy N., Qi Z., Ray P. Regulatory T cells in many flavors control asthma. Mucosal Immunol. 2010;3:216-229.
Not in our library10.1038/mi.2010.4
458.
Roncarolo M.G., Bacchetta R., Bordignon C., Narula S., Levings M.K. Type 1 T regulatory cells. Immunol. Rev. 2001;182:68-79.
Not in our library10.1034/j.1600-065x.2001.1820105.x
459.
Bocian K., Kiernozek E., Domagala-Kulawik J., Korczak-Kowalska G., Stelmaszczyk-Emmel A., Drela N. Expanding Diversity and Common Goal of Regulatory T and B Cells. I: Origin, Phenotype, Mechanisms. Arch. Immunol. Ther. Exp. (Warsz). 2017;65:501-520.
Not in our library10.1007/s00005-017-0469-3
460.
Weiner H.L. Induction and mechanism of action of transforming growth factor-beta-secreting Th3 regulatory cells. Immunol. Rev. 2001;182:207-214.
Not in our library10.1034/j.1600-065x.2001.1820117.x
461.
Chaudhry A., Samstein R.M., Treuting P., Liang Y., Pils M.C., Heinrich J.M., Jack R.S., Wunderlich F.T., Bruning J.C., Muller W., et al. Interleukin-10 signaling in regulatory T cells is required for suppression of Th17 cell-mediated inflammation. Immunity. 2011;34:566-578.
Not in our library10.1016/j.immuni.2011.03.018
462.
Hori S., Nomura T., Sakaguchi S. Control of regulatory T cell development by the transcription factor Foxp3. Science. 2003;299:1057-1061.
Not in our library10.1126/science.1079490
463.
Amin H.Z., Sasaki N., Hirata K.I. Regulatory T Cell Immunity in Atherosclerosis. Acta Med. Indones. 2017;49:63-68.
Not in our library
464.
Regulatory T Cells: Molecular Actions on Effector Cells in Immune Regulation · 2016
No notice
465.
Tselios K., Sarantopoulos A., Gkougkourelas I., Boura P. T regulatory cells: A promising new target in atherosclerosis. Crit. Rev. Immunol. 2014;34:389-397.
Not in our library10.1615/critrevimmunol.2014010802
466.
Wing K., Onishi Y., Prieto-Martin P., Yamaguchi T., Miyara M., Fehervari Z., Nomura T., Sakaguchi S. CTLA-4 control over Foxp3+ regulatory T cell function. Science. 2008;322:271-275.
Not in our library10.1126/science.1160062
467.
Gondek D.C., Lu L.F., Quezada S.A., Sakaguchi S., Noelle R.J. Cutting edge: Contact-mediated suppression by CD4+CD25+ regulatory cells involves a granzyme B-dependent, perforin-independent mechanism. J. Immunol. 2005;174:1783-1786.
Not in our library10.4049/jimmunol.174.4.1783
468.
Garin M.I., Chu C.C., Golshayan D., Cernuda-Morollon E., Wait R., Lechler R.I. Galectin-1: A key effector of regulation mediated by CD4+CD25+ T cells. Blood. 2007;109:2058-2065.
Not in our library10.1182/blood-2006-04-016451
469.
Ren X., Ye F., Jiang Z., Chu Y., Xiong S., Wang Y. Involvement of cellular death in TRAIL/DR5-dependent suppression induced by CD4(+)CD25(+) regulatory T cells. Cell Death Differ. 2007;14:2076-2084.
Not in our library10.1038/sj.cdd.4402220
470.
Li M.O., Flavell R.A. TGF-beta: A master of all T cell trades. Cell. 2008;134:392-404.
Not in our library10.1016/j.cell.2008.07.025
471.
Mallat Z., Besnard S., Duriez M., Deleuze V., Emmanuel F., Bureau M.F., Soubrier F., Esposito B., Duez H., Fievet C., et al. Protective role of interleukin-10 in atherosclerosis. Circ. Res. 1999;85:e17-e24.
Not in our library10.1161/01.res.85.8.e17
472.
Potteaux S., Esposito B., van Oostrom O., Brun V., Ardouin P., Groux H., Tedgui A., Mallat Z. Leukocyte-derived interleukin 10 is required for protection against atherosclerosis in low-density lipoprotein receptor knockout mice. Arterioscler. Thromb. Vasc. Biol. 2004;24:1474-1478.
Not in our library10.1161/01.atv.0000134378.86443.cd
473.
Mallat Z., Gojova A., Brun V., Esposito B., Fournier N., Cottrez F., Tedgui A., Groux H. Induction of a regulatory T cell type 1 response reduces the development of atherosclerosis in apolipoprotein E-knockout mice. Circulation. 2003;108:1232-1237.
Not in our library10.1161/01.cir.0000089083.61317.a1
474.
Sawant D.V., Hamilton K., Vignali D.A. Interleukin-35: Expanding Its Job Profile. J. Interferon Cytokine Res. 2015;35:499-512.
Not in our library10.1089/jir.2015.0015
475.
Collison L.W., Delgoffe G.M., Guy C.S., Vignali K.M., Chaturvedi V., Fairweather D., Satoskar A.R., Garcia K.C., Hunter C.A., Drake C.G., et al. The composition and signaling of the IL-35 receptor are unconventional. Nat. Immunol. 2012;13:290-299.
Not in our library10.1038/ni.2227
476.
Sha X., Meng S., Li X., Xi H., Maddaloni M., Pascual D.W., Shan H., Jiang X., Wang H., Yang X.F. Interleukin-35 Inhibits Endothelial Cell Activation by Suppressing MAPK-AP-1 Pathway. J. Biol. Chem. 2015;290:19307-19318.
Not in our library10.1074/jbc.m115.663286
477.
Li X., Fang P., Yang W.Y., Wang H., Yang X. IL-35, as a newly proposed homeostasis-associated molecular pattern, plays three major functions including anti-inflammatory initiator, effector, and blocker in cardiovascular diseases. Cytokine. 2017;122:154076.
Not in our library10.1016/j.cyto.2017.06.003
478.
Vignali D.A., Kuchroo V.K. IL-12 family cytokines: Immunological playmakers. Nat. Immunol. 2012;13:722-728.
Not in our library10.1038/ni.2366
479.
Wang R.X., Yu C.R., Dambuza I.M., Mahdi R.M., Dolinska M.B., Sergeev Y.V., Wingfield P.T., Kim S.H., Egwuagu C.E. Interleukin-35 induces regulatory B cells that suppress autoimmune disease. Nat. Med. 2014;20:633-641.
Not in our library10.1038/nm.3554
480.
Collison L.W., Vignali D.A. Interleukin-35: Odd one out or part of the family? Immunol. Rev. 2008;226:248-262.
Not in our library10.1111/j.1600-065x.2008.00704.x
481.
Collison L.W., Workman C.J., Kuo T.T., Boyd K., Wang Y., Vignali K.M., Cross R., Sehy D., Blumberg R.S., Vignali D.A. The inhibitory cytokine IL-35 contributes to regulatory T-cell function. Nature. 2007;450:566-569.
Not in our library10.1038/nature06306
482.
Interleukin 35: A Key Mediator of Suppression and the Propagation of Infectious Tolerance · 2013
No notice
483.
Kempe S., Heinz P., Kokai E., Devergne O., Marx N., Wirth T. Epstein-barr virus-induced gene-3 is expressed in human atheroma plaques. Am. J. Pathol. 2009;175:440-447.
Not in our library10.2353/ajpath.2009.080752
484.
Lin Y., Huang Y., Lu Z., Luo C., Shi Y., Zeng Q., Cao Y., Liu L., Wang X., Ji Q. Decreased plasma IL-35 levels are related to the left ventricular ejection fraction in coronary artery diseases. PLoS ONE. 2012;7:e52490.
Not in our library10.1371/journal.pone.0052490
485.
Tao L., Zhu J., Chen Y., Wang Q., Pan Y., Yu Q., Zhou B., Zhu H. IL-35 improves Treg-mediated immune suppression in atherosclerotic mice. Exp. Ther. Med. 2016;12:2469-2476.
Not in our library10.3892/etm.2016.3649
486.
Hirase T., Hara H., Miyazaki Y., Ide N., Nishimoto-Hazuku A., Fujimoto H., Saris C.J., Yoshida H., Node K. Interleukin 27 inhibits atherosclerosis via immunoregulation of macrophages in mice. Am. J. Physiol. Heart Circ. Physiol. 2013;305:H420-H429.
Not in our library10.1152/ajpheart.00198.2013
487.
Koltsova E.K., Kim G., Lloyd K.M., Saris C.J., von Vietinghoff S., Kronenberg M., Ley K. Interleukin-27 receptor limits atherosclerosis in Ldlr-/- mice. Circ. Res. 2012;111:1274-1285.
Not in our library10.1161/circresaha.112.277525
488.
Pandiyan P., Zheng L., Ishihara S., Reed J., Lenardo M.J. CD4+CD25+Foxp3+ regulatory T cells induce cytokine deprivation-mediated apoptosis of effector CD4+ T cells. Nat. Immunol. 2007;8:1353-1362.
Not in our library10.1038/ni1536
489.
Kobie J.J., Shah P.R., Yang L., Rebhahn J.A., Fowell D.J., Mosmann T.R. T regulatory and primed uncommitted CD4 T cells express CD73, which suppresses effector CD4 T cells by converting 5’-adenosine monophosphate to adenosine. J. Immunol. 2006;177:6780-6786.
Not in our library10.4049/jimmunol.177.10.6780
490.
Borsellino G., Kleinewietfeld M., Di Mitri D., Sternjak A., Diamantini A., Giometto R., Hopner S., Centonze D., Bernardi G., Dell’Acqua M.L., et al. Expression of ectonucleotidase CD39 by Foxp3+ Treg cells: Hydrolysis of extracellular ATP and immune suppression. Blood. 2007;110:1225-1232.
Not in our library10.1182/blood-2006-12-064527
491.
Zarek P.E., Huang C.T., Lutz E.R., Kowalski J., Horton M.R., Linden J., Drake C.G., Powell J.D. A2A receptor signaling promotes peripheral tolerance by inducing T-cell anergy and the generation of adaptive regulatory T cells. Blood. 2008;111:251-259.
Not in our library10.1182/blood-2007-03-081646
492.
Low Numbers of FOXP3 Positive Regulatory T Cells Are Present in all Developmental Stages of Human Atherosclerotic Lesions · 2007
No notice
493.
Wang Z., Mao S., Zhan Z., Yu K., He C., Wang C. Effect of hyperlipidemia on Foxp3 expression in apolipoprotein E-knockout mice. J. Cardiovasc. Med. (Hagerstown). 2014;15:273-279.
Not in our library10.2459/jcm.0b013e3283641b9c
494.
Ou H.X., Guo B.B., Liu Q., Li Y.K., Yang Z., Feng W.J., Mo Z.C. Regulatory T cells as a new therapeutic target for atherosclerosis. Acta Pharmacol. Sin. 2018;39:1249-1258.
Not in our library10.1038/aps.2017.140
495.
Sasaki N., Yamashita T., Kasahara K., Takeda M., Hirata K. Regulatory T cells and tolerogenic dendritic cells as critical immune modulators in atherogenesis. Curr. Pharm Des. 2015;21:1107-1117.
Not in our library10.2174/1381612820666141013142518
496.
Ait-Oufella H., Salomon B.L., Potteaux S., Robertson A.K., Gourdy P., Zoll J., Merval R., Esposito B., Cohen J.L., Fisson S., et al. Natural regulatory T cells control the development of atherosclerosis in mice. Nat. Med. 2006;12:178-180.
Not in our library10.1038/nm1343
497.
Lahl K., Loddenkemper C., Drouin C., Freyer J., Arnason J., Eberl G., Hamann A., Wagner H., Huehn J., Sparwasser T. Selective depletion of Foxp3+ regulatory T cells induces a scurfy-like disease. J. Exp. Med. 2007;204:57-63.
Not in our library10.1084/jem.20061852
498.
Klingenberg R., Gerdes N., Badeau R.M., Gistera A., Strodthoff D., Ketelhuth D.F., Lundberg A.M., Rudling M., Nilsson S.K., Olivecrona G., et al. Depletion of FOXP3+ regulatory T cells promotes hypercholesterolemia and atherosclerosis. J. Clin. Investig. 2013;123:1323-1334.
Not in our library10.1172/jci63891
499.
Steffens S., Burger F., Pelli G., Dean Y., Elson G., Kosco-Vilbois M., Chatenoud L., Mach F. Short-term treatment with anti-CD3 antibody reduces the development and progression of atherosclerosis in mice. Circulation. 2006;114:1977-1984.
Not in our library10.1161/circulationaha.106.627430
500.
Sasaki N., Yamashita T., Takeda M., Shinohara M., Nakajima K., Tawa H., Usui T., Hirata K. Oral anti-CD3 antibody treatment induces regulatory T cells and inhibits the development of atherosclerosis in mice. Circulation. 2009;120:1996-2005.
Not in our library10.1161/circulationaha.109.863431
501.
Dinh T.N., Kyaw T.S., Kanellakis P., To K., Tipping P., Toh B.H., Bobik A., Agrotis A. Cytokine therapy with interleukin-2/anti-interleukin-2 monoclonal antibody complexes expands CD4+CD25+Foxp3+ regulatory T cells and attenuates development and progression of atherosclerosis. Circulation. 2012;126:1256-1266.
Not in our library10.1161/circulationaha.112.099044
502.
Kasahara K., Sasaki N., Yamashita T., Kita T., Yodoi K., Sasaki Y., Takeda M., Hirata K. CD3 antibody and IL-2 complex combination therapy inhibits atherosclerosis by augmenting a regulatory immune response. J. Am. Heart Assoc. 2014;3:e000719.
Not in our library10.1161/jaha.113.000719
503.
Kita T., Yamashita T., Sasaki N., Kasahara K., Sasaki Y., Yodoi K., Takeda M., Nakajima K., Hirata K. Regression of atherosclerosis with anti-CD3 antibody via augmenting a regulatory T-cell response in mice. Cardiovasc. Res. 2014;102:107-117.
Not in our library10.1093/cvr/cvu002
504.
Sasaki N., Yamashita T., Kasahara K., Fukunaga A., Yamaguchi T., Emoto T., Yodoi K., Matsumoto T., Nakajima K., Kita T., et al. UVB Exposure Prevents Atherosclerosis by Regulating Immunoinflammatory Responses. Arterioscler. Thromb. Vasc. Biol. 2017;37:66-74.
Not in our library10.1161/atvbaha.116.308063
505.
Zhu Z.F., Meng K., Zhong Y.C., Qi L., Mao X.B., Yu K.W., Zhang W., Zhu P.F., Ren Z.P., Wu B.W., et al. Impaired circulating CD4+ LAP+ regulatory T cells in patients with acute coronary syndrome and its mechanistic study. PLoS ONE. 2014;9:e88775.
Not in our library10.1371/journal.pone.0088775
506.
Zhang W.C., Wang J., Shu Y.W., Tang T.T., Zhu Z.F., Xia N., Nie S.F., Liu J., Zhou S.F., Li J.J., et al. Impaired thymic export and increased apoptosis account for regulatory T cell defects in patients with non-ST segment elevation acute coronary syndrome. J. Biol. Chem. 2012;287:34157-34166.
Not in our library10.1074/jbc.m112.382978
507.
Wigren M., Bjorkbacka H., Andersson L., Ljungcrantz I., Fredrikson G.N., Persson M., Bryngelsson C., Hedblad B., Nilsson J. Low levels of circulating CD4+FoxP3+ T cells are associated with an increased risk for development of myocardial infarction but not for stroke. Arterioscler. Thromb. Vasc. Biol. 2012;32:2000-2004.
Not in our library10.1161/atvbaha.112.251579
508.
Ammirati E., Cianflone D., Banfi M., Vecchio V., Palini A., De Metrio M., Marenzi G., Panciroli C., Tumminello G., Anzuini A., et al. Circulating CD4+CD25hiCD127lo regulatory T-Cell levels do not reflect the extent or severity of carotid and coronary atherosclerosis. Arterioscler. Thromb. Vasc. Biol. 2010;30:1832-1841.
Not in our library10.1161/atvbaha.110.206813
509.
Mor A., Luboshits G., Planer D., Keren G., George J. Altered status of CD4(+)CD25(+) regulatory T cells in patients with acute coronary syndromes. Eur Heart J. 2006;27:2530-2537.
Not in our library10.1093/eurheartj/ehl222
510.
Emoto T., Sasaki N., Yamashita T., Kasahara K., Yodoi K., Sasaki Y., Matsumoto T., Mizoguchi T., Hirata K. Regulatory/effector T-cell ratio is reduced in coronary artery disease. Circ. J. 2014;78:2935-2941.
Not in our library10.1253/circj.cj-14-0644
511.
Regulation of Effector and Memory CD8 T Cell Differentiation by IL-2—A Balancing Act · 2018
No notice
512.
Andersen M.H., Schrama D., Thor Straten P., Becker J.C. Cytotoxic T cells. J. Invest. Dermatol. 2006;126:32-41.
Not in our library10.1038/sj.jid.5700001
513.
van Duijn J., Kuiper J., Slutter B. The many faces of CD8+ T cells in atherosclerosis. Curr. Opin. Lipidol. 2018;29:411-416.
Not in our library10.1097/mol.0000000000000541
514.
Kolbus D., Ljungcrantz I., Soderberg I., Alm R., Bjorkbacka H., Nilsson J., Fredrikson G.N. TAP1-deficiency does not alter atherosclerosis development in Apoe-/- mice. PLoS ONE. 2012;7:e33932.
Not in our library10.1371/journal.pone.0033932
515.
Fyfe A.I., Qiao J.H., Lusis A.J. Immune-deficient mice develop typical atherosclerotic fatty streaks when fed an atherogenic diet. J. Clin. Investig. 1994;94:2516-2520.
Not in our library10.1172/jci117622
516.
Chyu K.Y., Zhao X., Dimayuga P.C., Zhou J., Li X., Yano J., Lio W.M., Chan L.F., Kirzner J., Trinidad P., et al. CD8+ T cells mediate the athero-protective effect of immunization with an ApoB-100 peptide. PLoS ONE. 2012;7:e30780.
Not in our library10.1371/journal.pone.0030780
517.
Gewaltig J., Kummer M., Koella C., Cathomas G., Biedermann B.C. Requirements for CD8 T-cell migration into the human arterial wall. Hum. Pathol. 2008;39:1756-1762.
Not in our library10.1016/j.humpath.2008.04.018
518.
van Duijn J., van Elsas M., Benne N., Depuydt M., Wezel A., Smeets H., Bot I., Jiskoot W., Kuiper J., Slutter B. CD39 identifies a microenvironment-specific anti-inflammatory CD8(+) T-cell population in atherosclerotic lesions. Atherosclerosis. 2019;285:71-78.
Not in our library10.1016/j.atherosclerosis.2019.04.217
519.
Barquera S., Pedroza-Tobias A., Medina C., Hernandez-Barrera L., Bibbins-Domingo K., Lozano R., Moran A.E. Global Overview of the Epidemiology of Atherosclerotic Cardiovascular Disease. Arch. Med. Res. 2015;46:328-338.
Not in our library10.1016/j.arcmed.2015.06.006
520.
Kolbus D., Ramos O.H., Berg K.E., Persson J., Wigren M., Bjorkbacka H., Fredrikson G.N., Nilsson J. CD8+ T cell activation predominate early immune responses to hypercholesterolemia in Apoe(-)(/)(-) mice. BMC Immunol. 2010;11:58.
Not in our library10.1186/1471-2172-11-58
521.
Olofsson P.S., Soderstrom L.A., Wagsater D., Sheikine Y., Ocaya P., Lang F., Rabu C., Chen L., Rudling M., Aukrust P., et al. CD137 is expressed in human atherosclerosis and promotes development of plaque inflammation in hypercholesterolemic mice. Circulation. 2008;117:1292-1301.
Not in our library10.1161/circulationaha.107.699173
522.
Kyaw T., Winship A., Tay C., Kanellakis P., Hosseini H., Cao A., Li P., Tipping P., Bobik A., Toh B.H. Cytotoxic and proinflammatory CD8+ T lymphocytes promote development of vulnerable atherosclerotic plaques in apoE-deficient mice. Circulation. 2013;127:1028-1039.
Not in our library10.1161/circulationaha.112.001347
523.
Schatz D.G., Ji Y. Recombination centres and the orchestration of V(D)J recombination. Nat. Rev. Immunol. 2011;11:251-263.
Not in our library10.1038/nri2941
524.
Clark M.R., Mandal M., Ochiai K., Singh H. Orchestrating B cell lymphopoiesis through interplay of IL-7 receptor and pre-B cell receptor signalling. Nat. Rev. Immunol. 2014;14:69-80.
Not in our library10.1038/nri3570
525.
Nimmerjahn F., Ravetch J.V. Divergent immunoglobulin g subclass activity through selective Fc receptor binding. Science. 2005;310:1510-1512.
Not in our library10.1126/science.1118948
526.
Pillai S., Cariappa A. The follicular versus marginal zone B lymphocyte cell fate decision. Nat. Rev. Immunol. 2009;9:767-777.
Not in our library10.1038/nri2656
527.
Hardy R.R., Kincade P.W., Dorshkind K. The protean nature of cells in the B lymphocyte lineage. Immunity. 2007;26:703-714.
Not in our library10.1016/j.immuni.2007.05.013
528.
Hardy R.R. B-1 B cells: Development, selection, natural autoantibody and leukemia. Curr. Opin. Immunol. 2006;18:547-555.
Not in our library10.1016/j.coi.2006.07.010
529.
B-1 Cell Heterogeneity and the Regulation of Natural and Antigen-Induced IgM Production · 2016
No notice
530.
Choi Y.S., Dieter J.A., Rothaeusler K., Luo Z., Baumgarth N. B-1 cells in the bone marrow are a significant source of natural IgM. Eur. J. Immunol. 2012;42:120-129.
Not in our library10.1002/eji.201141890
531.
Berland R., Wortis H.H. Origins and functions of B-1 cells with notes on the role of CD5. Annu. Rev. Immunol. 2002;20:253-300.
Not in our library10.1146/annurev.immunol.20.100301.064833
532.
Srikakulapu P., McNamara C.A. B cells and atherosclerosis. Am. J. Physiol Heart Circ. Physiol. 2017;312:H1060-H1067.
Not in our library10.1152/ajpheart.00859.2016
533.
Roy B., Shukla S., Lyszkiewicz M., Krey M., Viegas N., Duber S., Weiss S. Somatic hypermutation in peritoneal B1b cells. Mol. Immunol. 2009;46:1613-1619.
Not in our library10.1016/j.molimm.2009.02.026
534.
An intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-β and retinoic acid. · 2013
Not checked
535.
Vaughan A.T., Roghanian A., Cragg M.S. B cells--masters of the immunoverse. Int. J. Biochem. Cell Biol. 2011;43:280-285.
Not in our library10.1016/j.biocel.2010.12.005
536.
Hamel K.M., Liarski V.M., Clark M.R. Germinal center B-cells. Autoimmunity. 2012;45:333-347.
Not in our library10.3109/08916934.2012.665524
537.
Shen P., Fillatreau S. Antibody-independent functions of B cells: A focus on cytokines. Nat. Rev. Immunol. 2015;15:441-451.
Not in our library10.1038/nri3857
538.
Lund F.E. Cytokine-producing B lymphocytes-key regulators of immunity. Curr. Opin. Immunol. 2008;20:332-338.
Not in our library10.1016/j.coi.2008.03.003
539.
Lund F.E., Garvy B.A., Randall T.D., Harris D.P. Regulatory roles for cytokine-producing B cells in infection and autoimmune disease. Curr. Dir. Autoimmun. 2005;8:25-54.
Not in our library10.1159/000082086
540.
Parekh V.V., Prasad D.V., Banerjee P.P., Joshi B.N., Kumar A., Mishra G.C. B cells activated by lipopolysaccharide, but not by anti-Ig and anti-CD40 antibody, induce anergy in CD8+ T cells: Role of TGF-beta 1. J. Immunol. 2003;170:5897-5911.
Not in our library10.4049/jimmunol.170.12.5897
541.
Tian J., Zekzer D., Hanssen L., Lu Y., Olcott A., Kaufman D.L. Lipopolysaccharide-activated B cells down-regulate Th1 immunity and prevent autoimmune diabetes in nonobese diabetic mice. J. Immunol. 2001;167:1081-1089.
Not in our library10.4049/jimmunol.167.2.1081
542.
Yanaba K., Bouaziz J.D., Haas K.M., Poe J.C., Fujimoto M., Tedder T.F. A regulatory B cell subset with a unique CD1dhiCD5+ phenotype controls T cell-dependent inflammatory responses. Immunity. 2008;28:639-650.
Not in our library10.1016/j.immuni.2008.03.017
543.
Caligiuri G., Nicoletti A., Poirier B., Hansson G.K. Protective immunity against atherosclerosis carried by B cells of hypercholesterolemic mice. J. Clin. Investig. 2002;109:745-753.
Not in our library10.1172/jci7272
544.
Major A.S., Fazio S., Linton M.F. B-lymphocyte deficiency increases atherosclerosis in LDL receptor-null mice. Arterioscler. Thromb. Vasc. Biol. 2002;22:1892-1898.
Not in our library10.1161/01.atv.0000039169.47943.ee
545.
Doran A.C., Lipinski M.J., Oldham S.N., Garmey J.C., Campbell K.A., Skaflen M.D., Cutchins A., Lee D.J., Glover D.K., Kelly K.A., et al. B-cell aortic homing and atheroprotection depend on Id3. Circ. Res. 2012;110:e1-e12.
Not in our library10.1161/circresaha.111.256438
546.
Palinski W., Miller E., Witztum J.L. Immunization of low density lipoprotein (LDL) receptor-deficient rabbits with homologous malondialdehyde-modified LDL reduces atherogenesis. Proc. Natl. Acad. Sci. USA. 1995;92:821-825.
Not in our library10.1073/pnas.92.3.821
547.
Ameli S., Hultgardh-Nilsson A., Regnstrom J., Calara F., Yano J., Cercek B., Shah P.K., Nilsson J. Effect of immunization with homologous LDL and oxidized LDL on early atherosclerosis in hypercholesterolemic rabbits. Arterioscler. Thromb. Vasc. Biol. 1996;16:1074-1079.
Not in our library10.1161/01.atv.16.8.1074
548.
Sage A.P., Tsiantoulas D., Baker L., Harrison J., Masters L., Murphy D., Loinard C., Binder C.J., Mallat Z. BAFF receptor deficiency reduces the development of atherosclerosis in mice--brief report. Arterioscler. Thromb. Vasc. Biol. 2012;32:1573-1576.
Not in our library10.1161/atvbaha.111.244731
549.
Kyaw T., Tay C., Khan A., Dumouchel V., Cao A., To K., Kehry M., Dunn R., Agrotis A., Tipping P., et al. Conventional B2 B cell depletion ameliorates whereas its adoptive transfer aggravates atherosclerosis. J. Immunol. 2010;185:4410-4419.
Not in our library10.4049/jimmunol.1000033
550.
Depletion of B2 but Not B1a B Cells in BAFF Receptor-Deficient ApoE−/− Mice Attenuates Atherosclerosis by Potently Ameliorating Arterial Inflammation · 2012
No notice
551.
Kyaw T., Cui P., Tay C., Kanellakis P., Hosseini H., Liu E., Rolink A.G., Tipping P., Bobik A., Toh B.H. BAFF receptor mAb treatment ameliorates development and progression of atherosclerosis in hyperlipidemic ApoE(-/-) mice. PLoS ONE. 2013;8:e60430.
Not in our library10.1371/journal.pone.0060430
552.
Ait-Oufella H., Herbin O., Bouaziz J.D., Binder C.J., Uyttenhove C., Laurans L., Taleb S., Van Vre E., Esposito B., Vilar J., et al. B cell depletion reduces the development of atherosclerosis in mice. J. Exp. Med. 2010;207:1579-1587.
Not in our library10.1084/jem.20100155
553.
Tsiantoulas D., Sage A.P., Goderle L., Ozsvar-Kozma M., Murphy D., Porsch F., Pasterkamp G., Menche J., Schneider P., Mallat Z., et al. B Cell-Activating Factor Neutralization Aggravates Atherosclerosis. Circulation. 2018;138:2263-2273.
Not in our library10.1161/circulationaha.117.032790
554.
Horkko S., Bird D.A., Miller E., Itabe H., Leitinger N., Subbanagounder G., Berliner J.A., Friedman P., Dennis E.A., Curtiss L.K., et al. Monoclonal autoantibodies specific for oxidized phospholipids or oxidized phospholipid-protein adducts inhibit macrophage uptake of oxidized low-density lipoproteins. J. Clin. Investig. 1999;103:117-128.
Not in our library10.1172/jci4533
555.
Lewis M.J., Malik T.H., Ehrenstein M.R., Boyle J.J., Botto M., Haskard D.O. Immunoglobulin M is required for protection against atherosclerosis in low-density lipoprotein receptor-deficient mice. Circulation. 2009;120:417-426.
Not in our library10.1161/circulationaha.109.868158
556.
Hosseini H., Li Y., Kanellakis P., Tay C., Cao A., Liu E., Peter K., Tipping P., Toh B.H., Bobik A., et al. Toll-Like Receptor (TLR)4 and MyD88 are Essential for Atheroprotection by Peritoneal B1a B Cells. J. Am. Heart Assoc. 2016;5:e002947.
Not in our library10.1161/jaha.115.002947
557.
Rosenfeld S.M., Perry H.M., Gonen A., Prohaska T.A., Srikakulapu P., Grewal S., Das D., McSkimming C., Taylor A.M., Tsimikas S., et al. B-1b Cells Secrete Atheroprotective IgM and Attenuate Atherosclerosis. Circ. Res. 2015;117:e28-e39.
Not in our library10.1161/circresaha.117.306044
558.
Bagchi-Chakraborty J., Francis A., Bray T., Masters L., Tsiantoulas D., Nus M., Harrison J., Broekhuizen M., Leggat J., Clatworthy M.R., et al. B Cell Fcgamma Receptor IIb Modulates Atherosclerosis in Male and Female Mice by Controlling Adaptive Germinal Center and Innate B-1-Cell Responses. Arterioscler. Thromb. Vasc. Biol. 2019;39:1379-1389.
Not in our library10.1161/atvbaha.118.312272
559.
Mizoguchi A., Mizoguchi E., Takedatsu H., Blumberg R.S., Bhan A.K. Chronic intestinal inflammatory condition generates IL-10-producing regulatory B cell subset characterized by CD1d upregulation. Immunity. 2002;16:219-230.
Not in our library10.1016/s1074-7613(02)00274-1
560.
Fillatreau S., Sweenie C.H., McGeachy M.J., Gray D., Anderton S.M. B cells regulate autoimmunity by provision of IL-10. Nat. Immunol. 2002;3:944-950.
Not in our library10.1038/ni833
561.
Mauri C., Gray D., Mushtaq N., Londei M. Prevention of arthritis by interleukin 10-producing B cells. J. Exp. Med. 2003;197:489-501.
Not in our library10.1084/jem.20021293
562.
Rattik S., Mantani P.T., Yao Mattisson I., Ljungcrantz I., Sundius L., Bjorkbacka H., Terrinoni M., Lebens M., Holmgren J., Nilsson J., et al. B cells treated with CTB-p210 acquire a regulatory phenotype in vitro and reduce atherosclerosis in apolipoprotein E deficient mice. Vascul. Pharmacol. 2018;111:54-61.
Not in our library10.1016/j.vph.2018.09.002
563.
Strom A.C., Cross A.J., Cole J.E., Blair P.A., Leib C., Goddard M.E., Rosser E.C., Park I., Hultgardh Nilsson A., Nilsson J., et al. B regulatory cells are increased in hypercholesterolaemic mice and protect from lesion development via IL-10. Thromb. Haemost. 2015;114:835-847.
Not in our library10.1160/th14-12-1084
564.
Ridker P.M., Everett B.M., Thuren T., MacFadyen J.G., Chang W.H., Ballantyne C., Fonseca F., Nicolau J., Koenig W., Anker S.D., et al. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease. N. Engl. J. Med. 2017;377:1119-1131.
Not in our library10.1056/nejmoa1707914
565.
Ridker P.M., Everett B.M., Pradhan A., MacFadyen J.G., Solomon D.H., Zaharris E., Mam V., Hasan A., Rosenberg Y., Iturriaga E., et al. Investigators, C. Low-Dose Methotrexate for the Prevention of Atherosclerotic Events. N. Engl. J. Med. 2019;380:752-762.
Not in our library10.1056/nejmoa1809798
566.
Everett B.M., Pradhan A.D., Solomon D.H., Paynter N., Macfadyen J., Zaharris E., Gupta M., Clearfield M., Libby P., Hasan A.A., et al. Rationale and design of the Cardiovascular Inflammation Reduction Trial: A test of the inflammatory hypothesis of atherothrombosis. Am. Heart J. 2013;166:199-207.
Not in our library10.1016/j.ahj.2013.03.018
567.
Palmer R.D., Vaccarezza M. New Promises and Challenges on Inflammation and Atherosclerosis: Insights From CANTOS and CIRT Trials. Front. Cardiovasc. Med. 2019;6:90.
Not in our library10.3389/fcvm.2019.00090

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A bibliometric analysis of T cell and atherosclerosis · 2022
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Innate Lymphoid Cells in Intestinal Homeostasis and Inflammatory Bowel Disease · 2021
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Endothelial Dysfunction, Inflammation and Coronary Artery Disease: Potential Biomarkers and Promising Therapeutical Approaches · 2021
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Bioinformatics analysis of vascular RNA-seq data revealed hub genes and pathways in a novel Tibetan minipig atherosclerosis model induced by a high fat/cholesterol diet · 2020
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