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Treatment of allergic asthma: Modulation of Th2 cells and their responses

Berislav Bosnjak, Barbara Stelzmueller, Klaus J Erb and 1 more

Respiratory Research · 2011 · Review

Abstract

Atopic asthma is a chronic inflammatory pulmonary disease characterised by recurrent episodes of wheezy, laboured breathing with an underlying Th2 cell-mediated inflammatory response in the airways. It is currently treated and, more or less, controlled depending on severity, with bronchodilators e.g. long-acting beta agonists and long-acting muscarinic antagonists or anti-inflammatory drugs such as corticosteroids (inhaled or oral), leukotriene modifiers, theophyline and anti-IgE therapy. Unfortunately, none of these treatments are curative and some asthmatic patients do not respond to intense anti-inflammatory therapies. Additionally, the use of long-term oral steroids has many undesired side effects. For this reason, novel and more effective drugs are needed. In this review, we focus on the CD4+ Th2 cells and their products as targets for the development of new drugs to add to the current armamentarium as adjuncts or as potential stand-alone treatments for allergic asthma. We argue that in early disease, the reduction or elimination of allergen-specific Th2 cells will reduce the consequences of repeated allergic inflammatory responses such as lung remodelling without causing generalised immunosuppression.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 22, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

1Asthma is a serious chronic inflammatory lung disease characterised by recurrent episodes of wheezy laboured breathing with prolonged expiration accompanied by dry coughing and viscous mucus. These symptoms result from bronchoconstriction, bronchial mucosal thickening by oedema, eosinophilic infiltration, bronchial wall remodelling and excessive mucus production with plugging of the conducting airways in the lungs. These airway changes lead to increased bronchial hyperreactivity to a variety of allergic and non-allergic stimuli. Obstruction is usually reversible, either spontaneously or in response to appropriate therapy. Asthma affects approximately 300 million people worldwide and can be fatal. Atopic or allergic asthma generally occurs in childhood or young adulthood (under the age of 40) in about 70-80% of cases and is caused by common allergens e.g. pollens, house dust, animal dander, inhalants, foods, drugs and occupationally encountered dust. Atopic asthma is characterised by detectable allergen-specific IgE and a positive skin test upon allergen provocation. The most severe chronic refractory asthma accounts for 5-10% of adults with asthma and is characterised by persistent symptoms and frequent exacerbations, despite treatment with high dose inhaled and/or oral corticosteroids and inhaled β2 adrenoceptor agonists. These patients are at greater risk of fatal and near-fatal exacerbations and display serious unremitting symptoms, resulting in a considerable impact on quality of life, disproportionate use of health care resources and adverse effects from regular systemic steroid use.

2The allergic immune response is a complex process beginning with the activation of allergen-specific Th2 cells by antigen presenting cells (APCs) followed by their proliferation, cytokine production, helper functions and the emergence of memory cells (Figure 1). The resulting pathophysiological response includes lung eosinophilic inflammation, oedema, smooth muscle contraction and increased mucus production, resulting in airway obstruction and eventual lung damage. Numerous experimental models and clinical studies support a central role of allergen-specific Th2 cells in pathophysiological responses. Although much is known about the pathogenesis of the disease, the mechanisms underlying Th2 cell differentiation and perpetuation remain unclear. Allergen-specific memory Th2 cells take up long-term residence within experimental mice after recovering from a single episode allergic asthma illustrated by the maintenance of elevated serum allergen-specific IgG1 and persistent inflammatory chronic lung infiltrates. Asthma exacerbations are induced by respiratory tract allergen challenge leading to pathology resembling patients. A reduction or elimination of specific Th2 responses permits the treatment of disease without causing generalised immunosuppression and makes it a prime target for disease abrogation. Although current asthma therapies (especially inhaled corticosteroids and β2-agonists) efficiently control the disease, development of novel drugs is crucial for disease control in patients with severe, corticosteroid-insensitive asthma, as well as for improvement of existing therapies in terms of a more favourable side effect profile. Additionally, the use of highly active drugs that reduce disease in the early stages may obviate the need for high dose steroids later on and may reduce the potential for unremitting, steroid-resistant disease. Current asthma therapies do not cure the disease and symptoms return soon after treatment is terminated. Treatment in the late stages of chronic, severe, unremitting allergic asthma may be too late. It is therefore, important to start treatment early to reduce disease. In the early stages of disease, allergen-specific Th2 memory cells appear to play an important role in initiating the immune response against the offending allergen. Eliminating these pathogenic cells at an early stage may lead to complete disease remission. There is a myriad of strategies to eliminate Th2 memory cells that are promising. This review focuses on these targets during the evolution of the Th2-mediated allergic immune response from allergen presentation to activation and survival of Th2 memory cells (Figure 1).

Improvement of existing anti-Th2 cell therapies

3Inhaled and oral corticosteroids, leukotriene modifiers, theophyline, anti-IgE and specific allergen immunotherapy (AI) are well-established treatments for asthma. Of these therapies, only AI specifically targets Th2 cells. AI is thought to function by either skewing the allergic Th2 response towards Th1 immunity or generating regulatory T cells (Tregs). While the mechanism remains controversial, AI is effective in a subset of patients. Classical immunotherapy or "allergy shots" in the last years is evolving towards non-injectable forms like subcutaneous and sublingual immunotherapy. Progress in AI focuses on the dose and nature of the allergens, with higher allergen doses improving AI effectiveness and chemically modified allergens (allergoids) increasing efficacy. The production of recombinant allergens of common allergens from DNA sequences that can be mutated, fragmented or chimerised leads to efficient hypoallergenic mixtures of allergens for treatment. Additionally important is the ability of producing T cell epitopes without B cell epitopes, which reduces adverse reactions or new technologies like covalently linked T cell epitopes, DNA vaccines encoding allergens, production of fusion proteins to increase allergen presentation, or expression of recombinant allergens in lactic bacteria able to colonise the gut. Equally promising is the production of random peptide libraries to determine structural equivalents, so called mimotopes, producing shorter peptides, though patients may develop de novo IgE antibodies against the treatment peptide. Although some novel adjuvants such as monophosphoryl lipid A from Salmonella minnesota or heat killed or live Mycobacterium tuberculosis did not meet expectations in clinical trials, other adjuvants like fusion proteins with bacterial surface layer components and cytosine-guanine dinucleotides (CpG) oligonucleotides (CpG-ODNs), as well as routes of allergen delivery, in oral microencapsulated forms or embedded in nanoparticles, are being explored.

Strategies to modulate antigen presentation and Th2 cell activation

4Dendritic cells (DCs) expressing CD11c+CD11b+, CD16+, CD141+ or CD8α predispose to allergic asthma. Sputum and bronchial biopsies of asthmatic patients contain higher DC numbers in comparison to healthy individuals and are increased after allergen exposure. Asthmatic DCs differ in cytokine, prostaglandin (PG), and chemokine synthesis and costimulatory molecule expression compared to healthy controls. In addition, allergen-pulsed DCs from asthmatic patients, but not healthy controls, preferentially stimulate T- cells to produce IL-4. DCs from asthmatics produce high amounts of PGE2, which decreases IL-12 and increases CCL17 and CCL22 production from DCs causing the polarisation of DCs, which promote Th2 cell differentiation and recruitment. Recently, thymic stromal lymphopoietin (TSLP) has emerged as a key mediator, which promotes DC-induced Th2 differentiation through the interaction of OX40:OX40L. Inhibition of DC-mediated antigen presentation represents a suitable treatment option for allergic diseases. While DCs are the most potent APCs, other cells also contribute to antigen presentation and may provide useful targets. Table 1 illustrates the cell type, target and mechanism of action for compounds and biologicals that reduce antigen presentation to Th2 cells and their subsequent activation.

Interference with Th2 differentiation and activation

5Antigen presentation induces clonal expansion and differentiation of naïve Th cells into mature Th1, Th2, Th17 or inducible Tregs [reviewed in]. Th2 cell polarisation is mediated by transcription factors, including GATA-3, which are crucial for Th2 lineage commitment. Initial signals that drive Th2 differentiation induce expression of the GATA-3, which mediates Th2 differentiation by inducing chromatin remodelling of Th2 gene loci, direct transactivation of Th2 gene expression and inhibition of IFNγ expression. Furthermore, GATA-3 expression must be sustained to maintain a Th2 phenotype. Beside other important factors, microRNAs have recently emerged as regulators of gene expression during differentiation and function [reviewed in]. Numerous microRNAs play important roles in asthma and selective inhibition of these molecules can be utilised to specifically target development of Th2 cells. Examples of other signal transduction pathway targets and their inhibitors are listed in Tables 2 and 3. Unfortunately, most of these targets are not selectively expressed in Th2 cells and their inhibitors have broad immunosuppressive effects.

Modulation of effector cytokines

6The interplay between cells and cytokines involved in Th2-mediated disease is complex. Th2 cells secrete and express a variety of cytokines and receptors. In the past decade, mAbs targeting the most prominent Th2 cytokines, IL-4, IL-5 and IL-13 have had variable success in clinical trials and the perception is that effectiveness will be improved by inhibiting two or all of them simultaneously. Furthermore, additional cytokines including IL-9 and IL-31 are secreted by Th2 cells and might represent novel or additive targets. Moreover, cytokines secreted by other cells such as Th1, Th17 and Tregs may suppress Th2 cell function. Importantly, augmenting suppressive effects and inhibiting disease-promoting effects of T cells may lead to new compounds. Table 4 illustrates examples of cytokines secreted by Th2 cells, have direct effects on Th2 differentiation or are involved in differentiation of other helper T cell subtypes that could inhibit Th2 cells.

Interference of Th2 cell homing and adhesion

7Chemokine-chemokine receptors (CKRs) are a complex system of 42 molecules and 19 receptors that orchestrate leukocyte migration in physiologic and pathologic conditions. Among CKRs, CCR4, CCR8, CXCR4 and CCR3 appear to be selectively expressed on Th2 lymphocytes making them potentially important specific Th2 cell targets. CCR4 regulates chemotaxis of Th2 cells and its ligands CCL17 and CCL22 are elevated in allergic asthma. Hence, selective CCR4 antagonists, such as bipiperidinyl carboxylic acid amides, or antibodies directed against CCR4 ligands could be promising treatments. However, CCR4 is also expressed on Tregs and cells with either Th1 or Th2 potential leading to CCR4 inhibitors causing immunosuppressive effects. CCR8 expression also appears to be increased in lung and airway Th2 cells in asthmatic patients. Airway eosinophilia and airway hyperresponsiveness (AHR), however, are not diminished in CCR8-/- mice and adoptively transferred Th2 cells not expressing CCR8 accumulate in the lungs. Despite these contrasting results, several CCR8 agonists and antagonists are in development and might help to clarify the role of CCR8 in disease pathogenesis. CXCR4 is also involved in Th2 cell migration into the lungs and treatment of allergic mice with selective CXCR4 inhibitors significantly reduces AHR and inflammatory responses, supporting the further development of CXCR4 antagonists for asthma treatment. CCR3, which regulates eosinophil and mast cell accumulation into the lungs, is expressed on Th2 lymphocytes. CCR3 inhibition is a promising Th2 cell target that reduces innate and adaptive allergic inflammation. TPI ASM8 is a compound that contains modified antisense oligonucleotides targeting CCR3 and the common beta chain of the receptors of GM-CSF, IL-5 and IL-13, decreases airway inflammation in humans after allergen exposure and is under clinical evaluation. Other CKRs that appear to regulate CD4+ T cell homing to the lungs in asthma include CCR5, CCR6, CCR7 and CXCR3. CCR7 is a CKR expressed on a large number of naïve and memory T cells and therefore does not represent suitable target. Expression of CCR5, CCR6 and CXCR3 is related to Th1 (CXCR3 and CCR5) or Th17 (CCR6) cells. Thus, it is possible that CKR agonists, rather than antagonists, might inhibit Th2 cells in asthma. Importantly, the chemokine system is highly redundant with promiscuous chemokine-CKR interactions, suggesting that a single chemokine or CKR could have compensatory mechanisms leading to unexpected side effects. Moreover, blocking of a single chemokine or CKR might also not have an effect due to this redundancy.

8CRTH2 is a mediator involved in the migration and activation of basophils, eosinophils and Th2 cells. CRTH2 inhibition leads to attenuated airway hyperreactivity and inflammation in animal models. Ramatroban, a dual thrombroxane A2 receptor (TP) and CRTH2 receptor antagonist, suppresses eosinophil chemotaxis in vitro and in vivo and is approved for the treatment of allergic rhinitis in Japan. Numerous other CRTH2 antagonists, such as 4-aminotetrahyrochinoline derivatives or indoleacetic acid derivatives, are currently under development and OC000459 is in clinical trials for the treatment of allergic asthma (ClinicalTrials.gov identifier: NCT01057927, NCT00890877). The CRTH2 receptor is a DP2 receptor. Biological effects of PGD2 and PGH2 are mediated by D prostanoid receptor 1 (DP1) and CRTH2 (DP2). PGD2 activates DP1, thereby affecting NK cells and their cytokine production into a profile more favourable for Th2 skewing. PGH2 is implicated in the accumulation of CRTH2+ cells at sites of inflammation. Additionally, as discussed above, PGE2 polarises DCs to promote Th2 cell differentiation and recruitment. These effects of PGE2 seem to be mediated by PGE2 receptor type 2 (EP2) and type 4 (EP4). Therefore, PGs and CRTH2 appear to be promising Th2 cell-specific targets.

9While homing receptors are important for Th2 cell migration, several adhesion molecules also play a role. For example, intercellular adhesion molecule (ICAM)-1 and ICAM-2 play important roles in T cell migration in the lungs and ICAM-1 deficiency reduces leukocyte infiltration into the airways, as well as IL-4 and IL-5 concentration in bronchoalveolar lavage fluid. Additionally, VCAM-1 plays a role in eosinophil migration and activation in addition to T cell trafficking. There are no clinical data to date for mAbs against ICAM-1 or VCAM-1 in the treatment of asthma. Other potential adhesion targets include VLA-4 (α4ß1 integrin) or P-, E- and L-selectins. Natalizumab blocks both α4ß1 and α4ß7 integrins, but was discontinued due to severe side -effects. Novel α4 integrin mAb LLP2A reduces AHR and inflammation in mouse allergic asthma. Unfortunately, initial results with VLA-4 antagonist GW559090 were disappointing, but newer and safer alternative VLA-4 antagonists are in development. Lastly, a pan-selectin inhibitor is currently in phase IIa clinical trials for COPD, might also be promising for asthma. None of these adhesion molecules is selectively expressed on Th2 cells.

10The anticoagulant heparin has anti-inflammatory properties that inhibit leukocyte extravasation. IVX-0142 is a heparin-derived hypersulfated disaccharide that appears to be well-tolerated and shows a trend towards attenuation of asthmatic responses, but does not affect AHR. Additional studies are needed to evaluate effects of these molecules on Th2 cells.

Inhibition of long-lived Th2 memory cells

11It is possible that long-lived Th2 memory cells establish anti-apoptotic mechanisms for long-term maintenance, which when inhibited may result in cell death. Interfering with mechanisms for their longevity in the lungs may eliminate Th2 cells. Corticosteroids, calcineurin inhibitors and the cysteine leukotriene receptor antagonist montelukast have pro-apoptotic effects on activated T cells, one of the many mechanisms that lead to their effectiveness in asthma. CX3CR1 seems to provide a survival signal for lung Th2 and Th1 cells, which when inhibited reduces allergic inflammation. T cells from p53-deficient mice have decreased apoptosis and increased Th2 differentiation, cytoxic lymphocyte antigen-4 (CTLA-4) promotes T cell apoptosis and CTLA-4-deficient Th cells are directed towards Th2 differentiation. Additionally, the ratio of anti-apoptotic protein Bcl-2 over pro-apoptotic protein Bax in peripheral blood lymphocytes of asthmatic patients is increased in comparison to healthy controls. Interestingly, Th2 cells express less Fas ligand (FasL) and are more resistant to apoptosis than other Th subtypes. Moreover, the Th2 cytokine IL-4 reduces FasL, while Th1 cytokines IFNγ, TGFβ and IL-2 increase FasL expression. Regulation of FasL plays an important role because FasL-expressing T cells are pivotal during the resolution of airway inflammation and intratracheal delivery of DCs co-transfected with FasL and allergen genes before allergen challenge-induced T cell apoptosis and decreased airway inflammation in mice. Induction of Fas expression on Th2 cells might be a possible treatment approach that would decrease their survival in the lungs despite the fact that Th2 cells are somewhat resistant to Fas-induced apoptosis. An additional important pathway for apoptosis in T cells involves granzyme B, which is critical for activation-induced cell death. Inhibition of granzyme B rescues Th2 cells from apoptosis, suggesting that selective activation of granzyme B in Th2 cells might be a novel target. Another possibility is that increased apoptosis of Tregs and their protection from apoptosis might be a method of treating disease but there is little information related to cell death of Tregs in allergic diseases and it is possible that dysregulated apoptosis of Tregs may contribute to allergic asthma.

New categories of targets: Statins and Rho kinases; TIM proteins; Galectins; Siglecs; Arginases; Histone deacetylase inhibitors; Pathogens and Toll-like receptors

12Statins are a class of cholesterol lowering drugs that also possess anti-inflammatory and immune properties. Simvastatin, Lovastatin and Pravastatin reduced eosinophilia and Th2 cytokines in animal models of asthma. Clinical trials evaluating Simvastatin (NCT00792337), Lovastatin (NCT00689806) and Atorvastatin (NCT00463827), are ongoing or completed, but data are not yet available. Some statins exert their action through regulation of Rho kinases, which are expressed at high levels in airway smooth muscle and regulate their contractility, but inhibition appears to impair lymphocyte cytokine secretion.

13The genes for the T cell immunoglobulin domain and mucin domain (TIM) proteins are encoded in the T cell and airway phenotype regulator region on chromosome 11. Initial results indicate that although TIM-1 is involved in Th2 cell differentiation and is associated with Th2-mediated diseases, it also regulates Th17 and Treg development. Furthermore, TIM proteins are expressed by other immune- cell types. Because TIM proteins do not exclusively regulate Th2 cells, they are less useful as targets than originally anticipated.

14Galectins are β-galactoside-binding proteins that bind to glycan residues on the surface of mammalian cells. Examples are Galectin-3 and -9, which appear to have numerous functions in T cell activation, differentiation and apoptosis. Airway inflammation and challenge is decreased in Galectin-3 knockout mice and intranasal administration of a plasmid encoding Galectin-3 abates chronic airway inflammation in a murine model of asthma. Galectin-9 binds to TIM-3, which is expressed on Th1 cells and is important for protective immunity against microbes and intravenous administration of Galectin-9 suppresses AHR and airway inflammation in a mouse model of asthma.

15Siglecs are sialic acid-recognising Ig-superfamily lectins. CD33-related Siglecs, which in humans include Siglec-3 and Siglecs-5 through -11, are predominantly found on human leukocytes and involved in innate immunity. Mouse Siglec-F, the equivalent of human Siglec-8, is expressed on eosinophils and regulates their apoptosis. Blocking Siglec-F function with a mAb reduces airway and lung eosinophilia in mice. Although Siglec-8 is a promising target directed against eosinophils, human T lymphocytes express little or no siglec molecules and do not appear to be a candidate for inhibiting Th2 cells.

16Arginase I and II are cationic amino acid transporters involved in the metabolism of basic amino acids expressed in inflammatory lesions of patients with allergic asthma. Arginase gene expression and enzyme activity are enhanced by IL-4 and IL-13. Inhibition of arginase I by RNA interference suppresses IL-13-mediated AHR in a murine model of asthma and inhalation of an arginase inhibitor decreases AHR and airway inflammation in a guinea pig model of asthma. Conversely, deletion of arginase in macrophages impairs their ability to suppress Th2-dependent inflammation and fibrosis. Further research is needed in order to clarify the role of arginases in Th2 immunity.

17Histone deacetylases (HDAC) appear to play an important role in cytokine transcription. Corticosteroid signalling requires HDAC2 to suppress inflammatory gene products and HDAC2 activity is diminished in corticosteroid-resistance. HDAC inhibitor Trichostatin A reduces allergic airway inflammation by decreasing expression of the Th2 cytokines, IL-4, IL-5 and IgE. In contrast, HDAC1 appears to be a negative regulator of Th2 cytokine expression. Chromatin modification enzymes might be potential targets for inhibition of Th2-mediated diseases.

18Many microbials or their proteins inhibit Th2 immune responses in murine models of asthma by polarising towards Th1 immunity or by generating suppressive Tregs. Interestingly, microbial agents have both time- and dose-dependent effects on allergic asthma. Certain allergens such as dust mite Der p2 and Der f2, bind LPS and are related to the MD-2 protein of the LPS-binding component of the TLR4 signalling complex, which might influence the induction of Th2 responses demonstrating a potential for microbials augmenting rather than reducing Th2 responses. Alternatively, bacterial DNA or chemically synthesised de novo unmethylated CpG are immunostimulatory ligands that bind to TLR9 and induce strong Th1 immune responses [reviewed in]. Such bacterial and synthetic DNA immunostimulatory oligonucleotides (ISS-ODNs) containing CpG motifs suppress Th2 responses during the sensitisation phase or immediately before challenge in experimental asthma [reviewed in]. They have therapeutic and prophylactic properties, including suppression of DC migration and co-stimulatory molecule expression and inhibition of IgE-dependent Th2 cytokine release from mast cells and basophils. Moreover, ISS-ODNs added to allergen immunotherapy significantly reduce clinical symptoms in patients with asthma.

Conclusions

19Th2 cells and/or their secreted effector molecules mediate the immune response to allergens and are triggered by exposure to specific allergens leading to allergic asthma. Thus, inhibiting or eliminating Th2 cells is a beneficial strategy for treating asthma as long as generalised immunosuppression is avoided. Additionally, it is especially important to consider targeting Th2 cells early in disease because when disease is chronic additional factors may cause perpetuation. Although there are a myriad of potential Th2 targets (Figure 2), the optimal, most effective anti-Th2 cell target for the clinic remains elusive.

20Aside from anti-IgE therapy for severe asthma, there are no major new drugs for the treatment of asthma in the last 20 years. The latest research in allergic asthma that has elucidated key factors governing Th2 immunity and identified potential targets is predominantly from animal models. Now, the challenge is to discover candidates, which best translate from animal models to patients. However, choosing the most effective new drug target candidate is especially difficult because human data is often lacking or incomplete. Additionally, the use of accurate, predictive biomarkers to evaluate Th2-modulating drugs such as FEV1, Quality of Life, reduction in steroid use, decrease allergen-induced late phase response and others are important to ensure that the efficacy/adverse effect profiles are standardised and enable easier decision-making for the best candidates. We would argue that the most promising new compounds for the clinic are those in which proof of concept in patients is established e.g. anti-IL-13 antibodies and CRTH2 antagonists. Other candidates currently tested in the clinic are anti-IL-5, anti-IL-4 and anti-IL-9 compounds and CCR4 antagonists. However, based on available human data, we suggest that the epithelial cell-derived cytokines TSLP, IL-25 and IL-33, which drive Th2 responses are the most promising candidates, with TLSP the clear frontrunner.

21Steroids are efficient for treating asthma because they inhibit numerous pro-inflammatory responses and induce numerous anti-inflammatory pathways. Thus, targeting a single mediator may not suffice for the treatment of allergic asthma because of the redundant immune and inflammatory pathways involved upon allergen challenge. Thus, we suggest that targeting more than one molecule simultaneously using dual specific antibody/protein platforms to engineer new drugs will be the next major approach in drug discovery. However, while this approach creates a scenario in which numerous targets can be combined, the caveat is that optimal candidates must be carefully chosen. Another important consideration for the therapeutic strategy for allergic asthma is that drugs may need to be developed for specific subtypes of disease in which particular cellular and molecular pathways drive the disease. One example is the anti-IL-5 mAb, which is only effective in asthmatics with very high sputum and lung eosinophil numbers. This example suggests that it is beneficial to better categorise patients and consider personalised medicine based on a clear classification of disease.

22These are exciting times for Th2 cell immunology as the results of basic research are defining key molecular and cellular components in the response to allergens. This information is already being converted to targets that are being tested in the clinic. Currently, irrespective of approach, we consider that a successful strategy for the treatment of allergic asthma will include a selective inhibition of Th2 cells with the ultimate aim of eliminating allergen-specific Th2 immune responses. We anticipate that new candidates will be approved in the near future and offer treatment options for patients suffering with asthma and other allergic diseases.

List of abbreviations

23AHR: Airway hyperresponsiveness; AI: Allergen immunotherapy; APC: Antigen presenting cell Bcl: B cell lymphoma; Th: CD4+ T helper; CKR: Chemokine receptor; CRTH2: Chemoattractant receptor-homologous molecule expressed on TH2 cells; CpG: Cytosine-guanine dinucleotides; CpG-ODN: Cytosine-phosphate-guanine oligonucleotides; CTLA-4: Cytoxic lymphocyte antigen- 4; DC: Dendritic cell; DP1: D prostanoid receptor 1; EGF: Epidermal growth factor; ERK: Extracellular signal regulated kinase FasL: Fas ligand; GM-CSF: Granulocyte-macrophage colony-stimulating factor; HDAC: Histone deacetylases; Ig: Immunoglobulin; ISS-ODNs: Immunostimulatory oligodeoxynucleotides; ICAM: Intercellular adhesion molecule; IFN: Interferon; IL: Interleukin; JAK: Janus kinase; JNK: Jun kinase mAb: monoclonal antibody; MAPK: Mitogen-activated protein kinases; PDE: Phosphodiesterase; PI3K: Phosphoinositide 3-kinase; PD-1: Programmed death-1; PG: Prostaglandin; Siglec: Sialic acid binding Ig-like lectins; STAT: Signal transducer and activator of transcription; SOCS: Suppressor of cytokine signalling; Treg: regulatory T cell; TSLP: Thymic stromal lymphopoietin; TLR: Toll-like receptor; TGF: Transforming growth factor; TNF: Tumour necrosis factor; VCAM: Vascular cell adhesion molecule; VLA: Very late antigen.

Competing interests

24Berislav Bosnjak - was employee of GlaxoSmithKline Research Centre Zagreb Ltd. until December 2008. No other competing interests.

25Barbara Stelzmüller - none

26Klaus J. Erb - is an employee of BoerhingerIngelheim Pharma, Respiratory Diseases Research, Biberach an der Riss, Germany

27Michelle M. Epstein - received funding from BoerhingerIngelheim Pharma, Respiratory Diseases Research, Biberach an der Riss, Germany for collaborative project

Authors' contributions

28BB - was involved in drafting the manuscript, revising it critically for important intellectual content; and has given final approval of the version to be published.

29BS - made substantial contributions to conception of the review, was involved in drafting the manuscript, revising it critically for important intellectual content; and has given final approval of the version to be published.

30KE - made substantial contributions to conception of the review, was involved in drafting the manuscript, revising it critically for important intellectual content; and has given final approval of the version to be published.

31ME - made substantial contributions to conception of the review, was involved in drafting the manuscript, revising it critically for important intellectual content; and has given final approval of the version to be published.

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Yerkovich ST Roponen M Smith ME McKenna K Bosco A Subrata LS Mamessier E Wikstrom ME Le Souef P Sly PD Allergen-enhanced thrombomodulin (blood dendritic cell antigen 3, CD141) expression on dendritic cells is associated with a TH2-skewed immune responseJ Allergy Clin Immunol2009 123209216e204
Not in our library10.1016/j.jaci.2008.09.009
28.
Hammad H de Vries VC Maldonado-Lopez R Moser M Maliszewski C Hoogsteden HC Lambrecht BN Differential capacity of CD8+ alpha or CD8- alpha dendritic cell subsets to prime for eosinophilic airway inflammation in the T-helper type 2-prone milieu of the lungClin Exp Allergy2004 3418341840
Not in our library10.1111/j.1365-2222.2004.02133.x
29.
Bertorelli G Bocchino V Zhou X Zanini A Bernini MV Damia R Di Comite V Grima P Olivieri D Dendritic cell number is related to IL-4 expression in the airways of atopic asthmatic subjectsAllergy2000 55449454
Not in our library10.1034/j.1398-9995.2000.055005449.x
30.
Moller GM Overbeek SE Van Helden-Meeuwsen CG Van Haarst JM Prens EP Mulder PG Postma DS Hoogsteden HC Increased numbers of dendritic cells in the bronchial mucosa of atopic asthmatic patients: downregulation by inhaled corticosteroidsClin Exp Allergy1996 26517524
Not in our library10.1111/j.1365-2222.1996.tb00571.x
31.
Bratke K Lommatzsch M Julius P Kuepper M Kleine HD Luttmann W Christian Virchow J Dendritic cell subsets in human bronchoalveolar lavage fluid after segmental allergen challengeThorax2007 62168175
Not in our library10.1136/thx.2006.067793
32.
Chen XQ Yang J Hu SP Nie HX Mao GY Chen HB Increased expression of CD86 and reduced production of IL-12 and IL-10 by monocyte-derived dendritic cells from allergic asthmatics and their effects on Th1- and Th2-type cytokine balanceRespiration2006 733440
Not in our library10.1159/000087457
33.
Hammad H Charbonnier AS Duez C Jacquet A Stewart GA Tonnel AB Pestel J Th2 polarization by Der p 1--pulsed monocyte-derived dendritic cells is due to the allergic status of the donorsBlood2001 9811351141
Not in our library10.1182/blood.v98.4.1135
34.
Long JA Fogel-Petrovic M Knight DA Thompson PJ Upham JW Higher prostaglandin e2 production by dendritic cells from subjects with asthma compared with normal subjectsAm J Respir Crit Care Med2004 170485491
Not in our library10.1164/rccm.200311-1595oc
35.
Hammad H Lambrecht BN Pochard P Gosset P Marquillies P Tonnel AB Pestel J Monocyte-derived dendritic cells induce a house dust mite-specific Th2 allergic inflammation in the lung of humanized SCID mice: involvement of CCR7J Immunol2002 16915241534
Not in our library10.4049/jimmunol.169.3.1524
36.
Kalinski P Schuitemaker JH Hilkens CM Kapsenberg ML Prostaglandin E2 induces the final maturation of IL-12-deficient CD1a+CD83+ dendritic cells: the levels of IL-12 are determined during the final dendritic cell maturation and are resistant to further modulationJ Immunol1998 16128042809
Not in our library
37.
McIlroy A Caron G Blanchard S Fremaux I Duluc D Delneste Y Chevailler A Jeannin P Histamine and prostaglandin E up-regulate the production of Th2-attracting chemokines (CCL17 and CCL22) and down-regulate IFN-gamma-induced CXCL10 production by immature human dendritic cellsImmunology2006 117507516
Not in our library10.1111/j.1365-2567.2006.02326.x
38.
Ito T Wang YH Duramad O Hori T Delespesse GJ Watanabe N Qin FX Yao Z Cao W Liu YJ TSLP-activated dendritic cells induce an inflammatory T helper type 2 cell response through OX40 ligandJ Exp Med2005 20212131223
Not in our library10.1084/jem.20051135
39.
Shi L Leu SW Xu F Zhou X Yin H Cai L Zhang L Local blockade of TSLP receptor alleviated allergic disease by regulating airway dendritic cellsClin Immunol2008 129202210
Not in our library10.1016/j.clim.2008.07.015
40.
Zhu J Paul WE CD4 T cells: fates, functions, and faultsBlood2008 11215571569
Not in our library10.1182/blood-2008-05-078154
41.
Zhang DH Cohn L Ray P Bottomly K Ray A Transcription factor GATA-3 is differentially expressed in murine Th1 and Th2 cells and controls Th2-specific expression of the interleukin-5 geneJ Biol Chem1997 2722159721603
Not in our library10.1074/jbc.272.34.21597
42.
Yamashita M Ukai-Tadenuma M Miyamoto T Sugaya K Hosokawa H Hasegawa A Kimura M Taniguchi M DeGregori J Nakayama T Essential role of GATA3 for the maintenance of type 2 helper T (Th2) cytokine production and chromatin remodeling at the Th2 cytokine gene lociJ Biol Chem2004 2792698326990
Not in our library10.1074/jbc.m403688200
43.
Pai SY Truitt ML Ho IC GATA-3 deficiency abrogates the development and maintenance of T helper type 2 cellsProc Natl Acad Sci USA2004 10119931998
Not in our library10.1073/pnas.0308697100
44.
Bi Y Liu G Yang R MicroRNAs: novel regulators during the immune responseJ Cell Physiol2009 218467472
Not in our library10.1002/jcp.21639
45.
Lodish HF Zhou B Liu G Chen CZ Micromanagement of the immune system by microRNAsNat Rev Immunol2008 8120130
Not in our library10.1038/nri2252
46.
MicroRNAs Profiling in Murine Models of Acute and Chronic Asthma: A Relationship with mRNAs Targets · 2011
No notice
47.
Bonecchi R Galliera E Borroni EM Corsi MM Locati M Mantovani A Chemokines and chemokine receptors: an overviewFront Biosci2009 14540551
Not in our library10.2741/3261
48.
Annunziato F Cosmi L Galli G Beltrame C Romagnani P Manetti R Romagnani S Maggi E Assessment of chemokine receptor expression by human Th1 and Th2 cells in vitro and in vivoJ Leukoc Biol1999 65691699
Not in our library10.1002/jlb.65.5.691
49.
Heijink IH Van Oosterhout AJ Strategies for targeting T-cells in allergic diseases and asthmaPharmacol Ther2006 112489500
Not in our library10.1016/j.pharmthera.2006.05.005
50.
Kuhn CF Bazin M Philippe L Zhang J Tylaska L Miret J Bauer PH Bipiperidinyl carboxylic acid amides as potent, selective, and functionally active CCR4 antagonistsChem Biol Drug Des2007 70268272
Not in our library10.1111/j.1747-0285.2007.00551.x
51.
Vijayanand P Durkin K Hartmann G Morjaria J Seumois G Staples KJ Hall D Bessant C Bartholomew M Howarth PH Chemokine receptor 4 plays a key role in T cell recruitment into the airways of asthmatic patientsJ Immunol2010 18445684574
Not in our library10.4049/jimmunol.0901342
52.
Woodfolk JA T-cell responses to allergensJ Allergy Clin Immunol2007 119280294quiz 295-286
Not in our library10.1016/j.jaci.2006.11.008
53.
Panina-Bordignon P Papi A Mariani M Di Lucia P Casoni G Bellettato C Buonsanti C Miotto D Mapp C Villa A The C-C chemokine receptors CCR4 and CCR8 identify airway T cells of allergen-challenged atopic asthmaticsJ Clin Invest2001 10713571364
Not in our library10.1172/jci12655
54.
Chung CD Kuo F Kumer J Motani AS Lawrence CE Henderson WR Jr Venkataraman C CCR8 is not essential for the development of inflammation in a mouse model of allergic airway diseaseJ Immunol2003 170581587
Not in our library10.4049/jimmunol.170.1.581
55.
Mikhak Z Fukui M Farsidjani A Medoff BD Tager AM Luster AD Contribution of CCR4 and CCR8 to antigen-specific T(H)2 cell trafficking in allergic pulmonary inflammationJ Allergy Clin Immunol2009 1236773e63
Not in our library10.1016/j.jaci.2008.09.049
56.
Fox JM Najarro P Smith GL Struyf S Proost P Pease JE Structure/function relationships of CCR8 agonists and antagonists. Amino-terminal extension of CCL1 by a single amino acid generates a partial agonistJ Biol Chem2006 2813665236661
Not in our library10.1074/jbc.m605584200
57.
Jin J Wang Y Wang F Kerns JK Vinader VM Hancock AP Lindon MJ Stevenson GI Morrow DM Rao P Oxazolidinones as novel human CCR8 antagonistsBioorg Med Chem Lett2007 1717221725
Not in our library10.1016/j.bmcl.2006.12.076
58.
Gonzalo JA Lloyd CM Peled A Delaney T Coyle AJ Gutierrez-Ramos JC Critical involvement of the chemotactic axis CXCR4/stromal cell-derived factor-1 alpha in the inflammatory component of allergic airway diseaseJ Immunol2000 165499508
Not in our library10.4049/jimmunol.165.1.499
59.
Hu JS Freeman CM Stolberg VR Chiu BC Bridger GJ Fricker SP Lukacs NW Chensue SW AMD3465, a novel CXCR4 receptor antagonist, abrogates schistosomal antigen-elicited (type-2) pulmonary granuloma formationAm J Pathol2006 169424432
Not in our library10.2353/ajpath.2006.051234
60.
Lukacs NW Berlin A Schols D Skerlj RT Bridger GJ AMD3100, a CxCR4 antagonist, attenuates allergic lung inflammation and airway hyperreactivityAm J Pathol2002 16013531360
Not in our library10.1016/s0002-9440(10)62562-x
61.
Humbles AA Lu B Friend DS Okinaga S Lora J Al-Garawi A Martin TR Gerard NP Gerard C The murine CCR3 receptor regulates both the role of eosinophils and mast cells in allergen-induced airway inflammation and hyperresponsivenessProc Natl Acad Sci USA2002 9914791484
Not in our library10.1073/pnas.261462598
62.
Sallusto F Mackay CR Lanzavecchia A Selective expression of the eotaxin receptor CCR3 by human T helper 2 cellsScience1997 27720052007
Not in our library10.1126/science.277.5334.2005
63.
Mori A Ogawa K Someya K Kunori Y Nagakubo D Yoshie O Kitamura F Hiroi T Kaminuma O Selective suppression of Th2-mediated airway eosinophil infiltration by low-molecular weight CCR3 antagonistsInt Immunol2007 19913921
Not in our library10.1093/intimm/dxm049
64.
Gauvreau GM Boulet LP Cockcroft DW Baatjes A Cote J Deschesnes F Davis B Strinich T Howie K Duong M Antisense therapy against CCR3 and the common beta chain attenuates allergen-induced eosinophilic responsesAm J Respir Crit Care Med2008 177952958
Not in our library10.1164/rccm.200708-1251oc
65.
Kallinich T Schmidt S Hamelmann E Fischer A Qin S Luttmann W Virchow JC Kroczek RA Chemokine-receptor expression on T cells in lung compartments of challenged asthmatic patientsClin Exp Allergy2005 352633
Not in our library10.1111/j.1365-2222.2004.02132.x
66.
Thomas SY Banerji A Medoff BD Lilly CM Luster AD Multiple chemokine receptors, including CCR6 and CXCR3, regulate antigen-induced T cell homing to the human asthmatic airwayJ Immunol2007 17919011912
Not in our library10.4049/jimmunol.179.3.1901
67.
Mionnet C Buatois V Kanda A Milcent V Fleury S Lair D Langelot M Lacoeuille Y Hessel E Coffman R CX3CR1 is required for airway inflammation by promoting T helper cell survival and maintenance in inflamed lungNat Med2010 1613051312
Not in our library10.1038/nm.2253
68.
Annunziato F Cosmi L Santarlasci V Maggi L Liotta F Mazzinghi B Parente E Fili L Ferri S Frosali F Phenotypic and functional features of human Th17 cellsJ Exp Med2007 20418491861
Not in our library10.1084/jem.20070663
69.
Pettipher R The roles of the prostaglandin D(2) receptors DP(1) and CRTH2 in promoting allergic responsesBr J Pharmacol2008 153Suppl 1S191199
Not in our library10.1038/sj.bjp.0707488
70.
Royer JF Schratl P Carrillo JJ Jupp R Barker J Weyman-Jones C Beri R Sargent C Schmidt JA Lang-Loidolt D Heinemann A A novel antagonist of prostaglandin D2 blocks the locomotion of eosinophils and basophilsEur J Clin Invest2008 38663671
Not in our library10.1111/j.1365-2362.2008.01989.x
71.
Lukacs NW Berlin AA Franz-Bacon K Sasik R Sprague LJ Ly TW Hardiman G Boehme SA Bacon KB CRTH2 antagonism significantly ameliorates airway hyperreactivity and downregulates inflammation-induced genes in a mouse model of airway inflammationAm J Physiol Lung Cell Mol Physiol2008 295L767779
Not in our library10.1152/ajplung.90351.2008
72.
Stebbins KJ Broadhead AR Correa LD Scott JM Truong YP Stearns BA Hutchinson JH Prasit P Evans JF Lorrain DS Therapeutic efficacy of AM156, a novel prostanoid DP2 receptor antagonist, in murine models of allergic rhinitis and house dust mite-induced pulmonary inflammationEur J Pharmacol2010 638142149
Not in our library10.1016/j.ejphar.2010.04.031
73.
Torres D Paget C Fontaine J Mallevaey T Matsuoka T Maruyama T Narumiya S Capron M Gosset P Faveeuw C Trottein F Prostaglandin D2 inhibits the production of IFN-gamma by invariant NK T cells: consequences in the control of B16 melanomaJ Immunol2008 180783792
Not in our library10.4049/jimmunol.180.2.783
74.
Schuligoi R Sedej M Waldhoer M Vukoja A Sturm EM Lippe IT Peskar BA Heinemann A Prostaglandin H2 induces the migration of human eosinophils through the chemoattractant receptor homologous molecule of Th2 cells, CRTH2J Leukoc Biol2009 85136145
Not in our library10.1189/jlb.0608387
75.
Tajima T Murata T Aritake K Urade Y Hirai H Nakamura M Ozaki H Hori M Lipopolysaccharide induces macrophage migration via prostaglandin D(2) and prostaglandin E(2)J Pharmacol Exp Ther2008 326493501
Not in our library10.1124/jpet.108.137992
76.
Porter JC Hall A Epithelial ICAM-1 and ICAM-2 regulate the egression of human T cells across the bronchial epitheliumFaseb J2009 23492502
Not in our library10.1096/fj.08-115899
77.
Furusho S Myou S Fujimura M Kita T Yasui M Kasahara K Nakao S Takehara K Sato S Role of intercellular adhesion molecule-1 in a murine model of toluene diisocyanate-induced asthmaClin Exp Allergy2006 3612941302
Not in our library10.1111/j.1365-2222.2006.02568.x
78.
Ueki S Kihara J Kato H Ito W Takeda M Kobayashi Y Kayaba H Chihara J Soluble vascular cell adhesion molecule-1 induces human eosinophil migrationAllergy2009 64718724
Not in our library10.1111/j.1398-9995.2008.01871.x
79.
Parmley LA Elkins ND Fini MA Liu YE Repine JE Wright RM Alpha-4/beta-1 and alpha-L/beta-2 integrins mediate cytokine induced lung leukocyte-epithelial adhesion and injuryBr J Pharmacol2007 152915929
Not in our library10.1038/sj.bjp.0707443
80.
Kelly M Hwang JM Kubes P Modulating leukocyte recruitment in inflammationJ Allergy Clin Immunol2007 120310
Not in our library10.1016/j.jaci.2007.05.017
81.
Mackay CR Moving targets: cell migration inhibitors as new anti-inflammatory therapiesNat Immunol2008 9988998
Not in our library10.1038/ni.f.210
82.
Kenyon NJ Liu R O'Roark EM Huang W Peng L Lam KS An alpha4 beta1 integrin antagonist decreases airway inflammation in ovalbumin-exposed miceEur J Pharmacol2009 603138146
Not in our library10.1016/j.ejphar.2008.11.063
83.
Ravensberg AJ Luijk B Westers P Hiemstra PS Sterk PJ Lammers JW Rabe KF The effect of a single inhaled dose of a VLA-4 antagonist on allergen-induced airway responses and airway inflammation in patients with asthmaAllergy2006 6110971103
Not in our library10.1111/j.1398-9995.2006.01146.x
84.
Davenport RJ Munday JR Alpha4-integrin antagonism--an effective approach for the treatment of inflammatory diseases?Drug Discov Today2007 12569576
Not in our library10.1016/j.drudis.2007.05.001
85.
Muro F Iimura S Yoneda Y Chiba J Watanabe T Setoguchi M Takayama G Yokoyama M Takashi T Nakayama A Machinaga N A novel and potent VLA-4 antagonist based on trans-4-substituted cyclohexanecarboxylic acidBioorg Med Chem2009 1712321243
Not in our library10.1016/j.bmc.2008.12.026
86.
Saku O Ohta K Arai E Nomoto Y Miura H Nakamura H Fuse E Nakasato Y Synthetic study of VLA-4/VCAM-1 inhibitors: synthesis and structure-activity relationship of piperazinylphenylalanine derivativesBioorg Med Chem Lett2008 1810531057
Not in our library10.1016/j.bmcl.2007.12.014
87.
Li JP Vlodavsky I Heparin, heparan sulfate and heparanase in inflammatory reactionsThromb Haemost2009 102823828
Not in our library10.1160/th09-02-0091
88.
Duong M Cockcroft D Boulet LP Ahmed T Iverson H Atkinson DC Stahl EG Watson R Davis B Milot J The effect of IVX-0142, a heparin-derived hypersulfated disaccharide, on the allergic airway responses in asthmaAllergy2008 6311951201
Not in our library10.1111/j.1398-9995.2008.01707.x
89.
Spinozzi F de Benedictis D de Benedictis FM Apoptosis, airway inflammation and anti-asthma therapy: from immunobiology to clinical applicationPediatr Allergy Immunol2008 19287295
Not in our library10.1111/j.1399-3038.2007.00668.x
90.
Simon HU Cell death in allergic diseasesApoptosis2009 14439446
Not in our library10.1007/s10495-008-0299-1
91.
Ohkusu-Tsukada K Tsukada T Isobe K Accelerated development and aging of the immune system in p53-deficient miceJ Immunol1999 16319661972
Not in our library
92.
Lee KM Chuang E Griffin M Khattri R Hong DK Zhang W Straus D Samelson LE Thompson CB Bluestone JA Molecular basis of T cell inactivation by CTLA-4Science1998 28222632266
Not in our library10.1126/science.282.5397.2263
93.
da Rocha Dias S Rudd CE CTLA-4 blockade of antigen-induced cell deathBlood2001 9711341137
Not in our library10.1182/blood.v97.4.1134
94.
Ubaldi V Gatta L Pace L Doria G Pioli C CTLA-4 engagement inhibits Th2 but not Th1 cell polarisationClin Dev Immunol2003 101317
Not in our library10.1080/10446670310001598519
95.
Changing survival, memory cell compartment, and T-helper balance of lymphocytes between severe and mild asthma · 2008
Not checked
96.
Ramsdell F Seaman MS Miller RE Picha KS Kennedy MK Lynch DH Differential ability of Th1 and Th2 T cells to express Fas ligand and to undergo activation-induced cell deathInt Immunol1994 615451553
Not in our library10.1093/intimm/6.10.1545
97.
Fang Y Yu S Ellis JS Sharav T Braley-Mullen H Comparison of sensitivity of Th1, Th2, and Th17 cells to Fas-mediated apoptosisJ Leukoc Biol2010 8710191028
Not in our library10.1189/jlb.0509352
98.
Tong J Clay BS Ferreira CM Bandukwala HS Moore TV Blaine KM Williams JW Hoffman LM Hamann KJ Shilling RA Fas ligand expression on T Cells is sufficient to prevent prolonged airway inflammation in a murine model of asthmaAm J Respir Cell Mol Biol2010 43342348
Not in our library10.1165/rcmb.2008-0454oc
99.
Wang Y Bi Y Wu K Wang C Dendritic cell co-transfected with FasL and allergen genes induces T cell tolerance and decreases airway inflammation in allergen induced murine modelMol Biol Rep2011 38809817
Not in our library10.1007/s11033-010-0170-7
100.
Devadas S Das J Liu C Zhang L Roberts AI Pan Z Moore PA Das G Shi Y Granzyme B is critical for T cell receptor-induced cell death of type 2 helper T cellsImmunity2006 25237247
Not in our library10.1016/j.immuni.2006.06.011
101.
Hothersall E McSharry C Thomson NC Potential therapeutic role for statins in respiratory diseaseThorax2006 61729734
Not in our library10.1136/thx.2005.057976
102.
Robinson AJ Kashanin D O'Dowd F Fitzgerald K Williams V Walsh GM Fluvastatin and lovastatin inhibit granulocyte macrophage-colony stimulating factor-stimulated human eosinophil adhesion to inter-cellular adhesion molecule-1 under flow conditionsClin Exp Allergy2009 3918661874
Not in our library10.1111/j.1365-2222.2009.03334.x
103.
Kim DY Ryu SY Lim JE Lee YS Ro JY Anti-inflammatory mechanism of simvastatin in mouse allergic asthma modelEur J Pharmacol2007 5577686
Not in our library10.1016/j.ejphar.2006.11.027
104.
Imamura M Okunishi K Ohtsu H Nakagome K Harada H Tanaka R Yamamoto K Dohi M Pravastatin attenuates allergic airway inflammation by suppressing antigen sensitisation, interleukin 17 production and antigen presentation in the lungThorax2009 644449
Not in our library10.1136/thx.2007.094540
105.
Chiba Y Arima J Sakai H Misawa M Lovastatin inhibits bronchial hyperresponsiveness by reducing RhoA signaling in rat allergic asthmaAm J Physiol Lung Cell Mol Physiol2008 294L705713
Not in our library10.1152/ajplung.00531.2007
106.
Zhou Q Liao JK Rho kinase: an important mediator of atherosclerosis and vascular diseaseCurr Pharm Des2009 1531083115
Not in our library10.2174/138161209789057986
107.
Schaafsma D Gosens R Zaagsma J Halayko AJ Meurs H Rho kinase inhibitors: a novel therapeutical intervention in asthma?Eur J Pharmacol2008 585398406
Not in our library10.1016/j.ejphar.2008.01.056
108.
Aihara M Dobashi K Iizuka K Nakazawa T Mori M Effect of Y-27632 on release of cytokines from peripheral T cells in asthmatic patients and normal subjectsInt Immunopharmacol2004 4557561
Not in our library10.1016/j.intimp.2003.12.014
109.
Lin J Kane LP Are TIM proteins involved in asthma development or pathology?Clinical and experimental allergy: journal of the British Society for Allergy and Clinical Immunology2011 41917919
Not in our library10.1111/j.1365-2222.2011.03771.x
110.
Su EW Lin JY Kane LP TIM-1 and TIM-3 proteins in immune regulationCytokine2008 44913
Not in our library10.1016/j.cyto.2008.06.013
111.
Kuchroo VK Dardalhon V Xiao S Anderson AC New roles for TIM family members in immune regulationNat Rev Immunol2008 8577580
Not in our library10.1038/nri2366
112.
Grigorian A Torossian S Demetriou M T-cell growth, cell surface organization, and the galectin-glycoprotein latticeImmunol Rev2009 230232246
Not in our library10.1111/j.1600-065x.2009.00796.x
113.
Ge XN Bahaie NS Kang BN Hosseinkhani MR Ha SG Frenzel EM Liu FT Rao SP Sriramarao P Allergen-induced airway remodeling is impaired in galectin-3-deficient miceJ Immunol2010 18512051214
Not in our library10.4049/jimmunol.1000039
114.
Lopez E del Pozo V Miguel T Sastre B Seoane C Civantos E Llanes E Baeza ML Palomino P Cardaba B Inhibition of chronic airway inflammation and remodeling by galectin-3 gene therapy in a murine modelJ Immunol2006 17619431950
Not in our library10.4049/jimmunol.176.3.1943
115.
Katoh S Ishii N Nobumoto A Takeshita K Dai SY Shinonaga R Niki T Nishi N Tominaga A Yamauchi A Hirashima M Galectin-9 inhibits CD44-hyaluronan interaction and suppresses a murine model of allergic asthmaAm J Respir Crit Care Med2007 1762735
Not in our library10.1164/rccm.200608-1243oc
116.
Varki A Angata T Siglecs--the major subfamily of I-type lectinsGlycobiology2006 161R27R
Not in our library10.1093/glycob/cwj126
117.
Angata T Margulies EH Green ED Varki A Large-scale sequencing of the CD33-related Siglec gene cluster in five mammalian species reveals rapid evolution by multiple mechanismsProceedings of the National Academy of Sciences of the United States of America2004 1011325113256
Not in our library10.1073/pnas.0404833101
118.
Zhang M Angata T Cho JY Miller M Broide DH Varki A Defining the in vivo function of Siglec-F, a CD33-related Siglec expressed on mouse eosinophilsBlood2007 10942804287
Not in our library10.1182/blood-2006-08-039255
119.
Song DJ Cho JY Lee SY Miller M Rosenthal P Soroosh P Croft M Zhang M Varki A Broide DH Anti-Siglec-F antibody reduces allergen-induced eosinophilic inflammation and airway remodelingJournal of immunology2009 18353335341
Not in our library10.4049/jimmunol.0801421
120.
Nguyen DH Hurtado-Ziola N Gagneux P Varki A Loss of Siglec expression on T lymphocytes during human evolutionProceedings of the National Academy of Sciences of the United States of America2006 10377657770
Not in our library10.1073/pnas.0510484103
121.
King NE Rothenberg ME Zimmermann N Arginine in asthma and lung inflammationJ Nutr2004 1342830S2836Sdiscussion 2853S
Not in our library10.1093/jn/134.10.2830s
122.
Maarsingh H Zaagsma J Meurs H Arginase: a key enzyme in the pathophysiology of allergic asthma opening novel therapeutic perspectivesBr J Pharmacol2009 158652664
Not in our library10.1111/j.1476-5381.2009.00374.x
123.
Zimmermann N King NE Laporte J Yang M Mishra A Pope SM Muntel EE Witte DP Pegg AA Foster PS Dissection of experimental asthma with DNA microarray analysis identifies arginase in asthma pathogenesisJ Clin Invest2003 11118631874
Not in our library10.1172/jci17912
124.
Yang M Rangasamy D Matthaei KI Frew AJ Zimmmermann N Mahalingam S Webb DC Tremethick DJ Thompson PJ Hogan SP Inhibition of arginase I activity by RNA interference attenuates IL-13-induced airways hyperresponsivenessJ Immunol2006 17755955603
Not in our library10.4049/jimmunol.177.8.5595
125.
Arginase-1–Expressing Macrophages Suppress Th2 Cytokine–Driven Inflammation and Fibrosis · 2009
No notice
126.
Su RC Becker AB Kozyrskyj AL Hayglass KT Epigenetic regulation of established human type 1 versus type 2 cytokine responsesJ Allergy Clin Immunol2008 1215763e53
Not in our library10.1016/j.jaci.2007.09.004
127.
Choi JH Oh SW Kang MS Kwon HJ Oh GT Kim DY Trichostatin A attenuates airway inflammation in mouse asthma modelClin Exp Allergy2005 358996
Not in our library10.1111/j.1365-2222.2004.02006.x
128.
Grausenburger R Bilic I Boucheron N Zupkovitz G El-Housseiny L Tschismarov R Zhang Y Rembold M Gaisberger M Hartl A Conditional deletion of histone deacetylase 1 in T cells leads to enhanced airway inflammation and increased Th2 cytokine productionJ Immunol2010 18534893497
Not in our library10.4049/jimmunol.0903610
129.
Debarry J Garn H Hanuszkiewicz A Dickgreber N Blumer N von Mutius E Bufe A Gatermann S Renz H Holst O Heine H Acinetobacter lwoffii and Lactococcus lactis strains isolated from farm cowsheds possess strong allergy-protective propertiesJ Allergy Clin Immunol2007 11915141521
Not in our library10.1016/j.jaci.2007.03.023
130.
Smit JJ Folkerts G Nijkamp FP Mycobacteria, genes and the 'hygiene hypothesis'Curr Opin Allergy Clin Immunol2004 45762
Not in our library10.1097/00130832-200402000-00012
131.
Christ AP Rodriguez D Bortolatto J Borducchi E Keller A Mucida D Silva JS Leite LC Russo M Enhancement of Th1 Lung Immunity Induced by Recombinant Mycobacterium bovis BCG Attenuates Airway Allergic DiseaseAm J Respir Cell Mol Biol2009
Not in our library10.1165/rcmb.2009-0040oc
132.
Yokoi T Amakawa R Tanijiri T Sugimoto H Torii Y Amuro H Son Y Tajima K Liu YJ Ito T Fukuhara S Mycobacterium bovis Bacillus Calmette-Guerin suppresses inflammatory Th2 responses by inducing functional alteration of TSLP-activated dendritic cellsInt Immunol2008 2013211329
Not in our library10.1093/intimm/dxn094
133.
Ou-Yang HF Hu XB Ti XY Shi JR Li SJ Qi HW Wu CG Suppression of allergic airway inflammation in a mouse model by Der p2 recombined BCGImmunology2009 128e343352
Not in our library10.1111/j.1365-2567.2008.02970.x
134.
Wu Q Martin RJ Lafasto S Chu HW A low dose of Mycoplasma pneumoniae infection enhances an established allergic inflammation in mice: the role of the prostaglandin E2 pathwayClin Exp Allergy2009 3917541763
Not in our library10.1111/j.1365-2222.2009.03309.x
135.
Delayre-Orthez C de Blay F Frossard N Pons F Dose-dependent effects of endotoxins on allergen sensitization and challenge in the mouseClin Exp Allergy2004 3417891795
Not in our library10.1111/j.1365-2222.2004.02082.x
136.
Ichikawa S Takai T Yashiki T Takahashi S Okumura K Ogawa H Kohda D Hatanaka H Lipopolysaccharide binding of the mite allergen Der f 2Genes Cells2009 1410551065
Not in our library10.1111/j.1365-2443.2009.01334.x
137.
Inohara N Nunez G ML -- a conserved domain involved in innate immunity and lipid metabolismTrends Biochem Sci2002 27219221
Not in our library10.1016/s0968-0004(02)02084-4
138.
Klinman D Shirota H Tross D Sato T Klaschik S Synthetic oligonucleotides as modulators of inflammationJ Leukoc Biol2008 84958964
Not in our library10.1189/jlb.1107775
139.
Fonseca DE Kline JN Use of CpG oligonucleotides in treatment of asthma and allergic diseaseAdv Drug Deliv Rev2009 61256262
Not in our library10.1016/j.addr.2008.12.007
140.
Sur S Wild JS Choudhury BK Sur N Alam R Klinman DM Long term prevention of allergic lung inflammation in a mouse model of asthma by CpG oligodeoxynucleotidesJ Immunol1999 16262846293
Not in our library
141.
Constabel H Stankov MV Hartwig C Tschernig T Behrens GM Impaired lung dendritic cell migration and T cell stimulation induced by immunostimulatory oligonucleotides contribute to reduced allergic airway inflammationJ Immunol2009 18334433453
Not in our library10.4049/jimmunol.0804223
142.
Hessel EM Chu M Lizcano JO Chang B Herman N Kell SA Wills-Karp M Coffman RL Immunostimulatory oligonucleotides block allergic airway inflammation by inhibiting Th2 cell activation and IgE-mediated cytokine inductionJ Exp Med2005 20215631573
Not in our library10.1084/jem.20050631
143.
Senti G Johansen P Haug S Bull C Gottschaller C Muller P Pfister T Maurer P Bachmann MF Graf N Kundig TM Use of A-type CpG oligodeoxynucleotides as an adjuvant in allergen-specific immunotherapy in humans: a phase I/IIa clinical trialClin Exp Allergy2009 39562570
Not in our library10.1111/j.1365-2222.2008.03191.x
144.
Angeli V Hammad H Staels B Capron M Lambrecht BN Trottein F Peroxisome proliferator-activated receptor gamma inhibits the migration of dendritic cells: consequences for the immune responseJ Immunol2003 17052955301
Not in our library10.4049/jimmunol.170.10.5295
145.
Hammad H de Heer HJ Soullie T Angeli V Trottein F Hoogsteden HC Lambrecht BN Activation of peroxisome proliferator-activated receptor-gamma in dendritic cells inhibits the development of eosinophilic airway inflammation in a mouse model of asthmaAm J Pathol2004 164263271
Not in our library10.1016/s0002-9440(10)63116-1
146.
Hutchison S Choo-Kang BS Gibson VB Bundick RV Leishman AJ Brewer JM McInnes IB Garside P An investigation of the impact of the location and timing of antigen-specific T cell division on airways inflammationClin Exp Immunol2009 155107116
Not in our library10.1111/j.1365-2249.2008.03800.x
147.
Idzko M Hammad H van Nimwegen M Kool M Muller T Soullie T Willart MA Hijdra D Hoogsteden HC Lambrecht BN Local application of FTY720 to the lung abrogates experimental asthma by altering dendritic cell functionJ Clin Invest2006 11629352944
Not in our library10.1172/jci28295
148.
Nishiuma T Nishimura Y Okada T Kuramoto E Kotani Y Jahangeer S Nakamura S Inhalation of sphingosine kinase inhibitor attenuates airway inflammation in asthmatic mouse modelAm J Physiol Lung Cell Mol Physiol2008 294L10851093
Not in our library10.1152/ajplung.00445.2007
149.
Sawicka E Zuany-Amorim C Manlius C Trifilieff A Brinkmann V Kemeny DM Walker C Inhibition of Th1- and Th2-mediated airway inflammation by the sphingosine 1-phosphate receptor agonist FTY720J Immunol2003 17162066214
Not in our library10.4049/jimmunol.171.11.6206
150.
Xia M Sui Z Recent developments in CCR2 antagonistsExpert Opin Ther Pat2009 19295303
Not in our library10.1517/13543770902755129
151.
Pichavant M Charbonnier AS Taront S Brichet A Wallaert B Pestel J Tonnel AB Gosset P Asthmatic bronchial epithelium activated by the proteolytic allergen Der p 1 increases selective dendritic cell recruitmentJ Allergy Clin Immunol2005 115771778
Not in our library10.1016/j.jaci.2004.11.043
152.
Ip WK Wong CK Lam CW Interleukin (IL)-4 and IL-13 up-regulate monocyte chemoattractant protein-1 expression in human bronchial epithelial cells: involvement of p38 mitogen-activated protein kinase, extracellular signal-regulated kinase 1/2 and Janus kinase-2 but not c-Jun NH2-terminal kinase 1/2 signalling pathwaysClin Exp Immunol2006 145162172
Not in our library10.1111/j.1365-2249.2006.03085.x
153.
Hammad H Kool M Soullie T Narumiya S Trottein F Hoogsteden HC Lambrecht BN Activation of the D prostanoid 1 receptor suppresses asthma by modulation of lung dendritic cell function and induction of regulatory T cellsJ Exp Med2007 204357367
Not in our library10.1084/jem.20061196
154.
Crosby JR Guha M Tung D Miller DA Bender B Condon TP York-DeFalco C Geary RS Monia BP Karras JG Gregory SA Inhaled CD86 antisense oligonucleotide suppresses pulmonary inflammation and airway hyper-responsiveness in allergic miceJ Pharmacol Exp Ther2007 321938946
Not in our library10.1124/jpet.106.119214
155.
Yokomura K Suda T Matsuda H Hashizume H Asada K Suzuki K Chida K Suplatast tosilate alters DC1/DC2 balance in peripheral blood in bronchial asthmaJ Asthma2005 42567570
Not in our library10.1080/02770900500215913
156.
Chen YQ Shi HZ CD28/CTLA-4--CD80/CD86 and ICOS--B7RP-1 costimulatory pathway in bronchial asthmaAllergy2006 611526
Not in our library10.1111/j.1398-9995.2006.01008.x
157.
Seshasayee D Lee WP Zhou M Shu J Suto E Zhang J Diehl L Austin CD Meng YG Tan M In vivo blockade of OX40 ligand inhibits thymic stromal lymphopoietin driven atopic inflammationJ Clin Invest2007 11738683878
Not in our library10.1172/jci33559
158.
Singh AK Stock P Akbari O Role of PD-L1 and PD-L2 in allergic diseases and asthmaAllergy2011 66155162
Not in our library10.1111/j.1398-9995.2010.02458.x
159.
Tilley SL Boucher RC A1 antagonism in asthma: better than coffee?J Clin Invest2005 1151316
Not in our library10.1172/jci24009
160.
Lopez-Castejon G Baroja-Mazo A Pelegrin P Novel macrophage polarization model: from gene expression to identification of new anti-inflammatory moleculesCell Mol Life Sci2010
Not in our library10.1007/s00018-010-0609-y
161.
Chen CL Wang YM Liu CF Wang JY The effect of water-soluble chitosan on macrophage activation and the attenuation of mite allergen-induced airway inflammationBiomaterials2008 2921732182
Not in our library10.1016/j.biomaterials.2008.01.023
162.
Korf JE Pynaert G Tournoy K Boonefaes T Van Oosterhout A Ginneberge D Haegeman A Verschoor JA De Baetselier P Grooten J Macrophage reprogramming by mycolic acid promotes a tolerogenic response in experimental asthmaAm J Respir Crit Care Med2006 174152160
Not in our library10.1164/rccm.200507-1175oc
163.
Perrigoue JG Saenz SA Siracusa MC Allenspach EJ Taylor BC Giacomin PR Nair MG Du Y Zaph C van Rooijen N MHC class II-dependent basophil-CD4+ T cell interactions promote T(H)2 cytokine-dependent immunityNat Immunol2009 10697705
Not in our library10.1038/ni.1740
164.
Sokol CL Barton GM Farr AG Medzhitov R A mechanism for the initiation of allergen-induced T helper type 2 responsesNat Immunol2008 9310318
Not in our library10.1038/ni1558
165.
Sokol CL Chu NQ Yu S Nish SA Laufer TM Medzhitov R Basophils function as antigen-presenting cells for an allergen-induced T helper type 2 responseNat Immunol2009 10713720
Not in our library10.1038/ni.1738
166.
Yoshimoto T Yasuda K Tanaka H Nakahira M Imai Y Fujimori Y Nakanishi K Basophils contribute to T(H)2-IgE responses in vivo via IL-4 production and presentation of peptide-MHC class II complexes to CD4+ T cellsNat Immunol2009 10706712
Not in our library10.1038/ni.1737
167.
Hammad H Plantinga M Deswarte K Pouliot P Willart MA Kool M Muskens F Lambrecht BN Inflammatory dendritic cells--not basophils--are necessary and sufficient for induction of Th2 immunity to inhaled house dust mite allergenJ Exp Med2010 20720972111
Not in our library10.1084/jem.20101563
168.
Kim S Prout M Ramshaw H Lopez AF LeGros G Min B Cutting edge: basophils are transiently recruited into the draining lymph nodes during helminth infection via IL-3, but infection-induced Th2 immunity can develop without basophil lymph node recruitment or IL-3Journal of immunology2010 18411431147
Not in our library10.4049/jimmunol.0902447
169.
Ho IC Tai TS Pai SY GATA3 and the T-cell lineage: essential functions before and after T-helper-2-cell differentiationNat Rev Immunol2009 9125135
Not in our library10.1038/nri2476
170.
Finotto S De Sanctis GT Lehr HA Herz U Buerke M Schipp M Bartsch B Atreya R Schmitt E Galle PR Treatment of allergic airway inflammation and hyperresponsiveness by antisense-induced local blockade of GATA-3 expressionJ Exp Med2001 19312471260
Not in our library10.1084/jem.193.11.1247
171.
Lee CC Huang HY Chiang BL Lentiviral-mediated GATA-3 RNAi decreases allergic airway inflammation and hyperresponsivenessMol Ther2008 166065
Not in our library10.1038/sj.mt.6300309
172.
Stritesky GL Muthukrishnan R Sehra S Goswami R Pham D Travers J Nguyen ET Levy DE Kaplan MH The transcription factor STAT3 is required for T helper 2 cell developmentImmunity2011 343949
Not in our library10.1016/j.immuni.2010.12.013
173.
Simeone-Penney MC Severgnini M Tu P Homer RJ Mariani TJ Cohn L Simon AR Airway epithelial STAT3 is required for allergic inflammation in a murine model of asthmaJ Immunol2007 17861916199
Not in our library10.4049/jimmunol.178.10.6191
174.
Kagami S Nakajima H Kumano K Suzuki K Suto A Imada K Davey HW Saito Y Takatsu K Leonard WJ Iwamoto I Both stat5a and stat5b are required for antigen-induced eosinophil and T-cell recruitment into the tissueBlood2000 9513701377
Not in our library
175.
D'Cruz LM Klein L Development and function of agonist-induced CD25+Foxp3+ regulatory T cells in the absence of interleukin 2 signalingNat Immunol2005 611521159
Not in our library10.1038/ni1264
176.
Ohga K Kuromitsu S Takezawa R Numazaki M Ishikawa J Nagashima S Shimizu Y YM-341619 suppresses the differentiation of spleen T cells into Th2 cells in vitro, eosinophilia, and airway hyperresponsiveness in rat allergic modelsEur J Pharmacol2008 590409416
Not in our library10.1016/j.ejphar.2008.06.035
177.
Walker W Healey GD Hopkin JM RNA interference of STAT6 rapidly attenuates ongoing interleukin-13-mediated events in lung epithelial cellsImmunology2009 127256266
Not in our library10.1111/j.1365-2567.2008.02951.x
178.
Amsen D Antov A Jankovic D Sher A Radtke F Souabni A Busslinger M McCright B Gridley T Flavell RA Direct regulation of Gata3 expression determines the T helper differentiation potential of NotchImmunity2007 278999
Not in our library10.1016/j.immuni.2007.05.021
179.
Fang TC Yashiro-Ohtani Y Del Bianco C Knoblock DM Blacklow SC Pear WS Notch directly regulates Gata3 expression during T helper 2 cell differentiationImmunity2007 27100110
Not in our library10.1016/j.immuni.2007.04.018
180.
Kang JH Kim BS Uhm TG Lee SH Lee GR Park CS Chung IY Gamma-secretase inhibitor reduces allergic pulmonary inflammation by modulating Th1 and Th2 responsesAm J Respir Crit Care Med2009 179875882
Not in our library10.1164/rccm.200806-893oc
181.
Tu L Fang TC Artis D Shestova O Pross SE Maillard I Pear WS Notch signaling is an important regulator of type 2 immunityJ Exp Med2005 20210371042
Not in our library10.1084/jem.20050923
182.
Kovall RA More complicated than it looks: assembly of Notch pathway transcription complexesOncogene2008 2750995109
Not in our library10.1038/onc.2008.223
183.
Fortini ME Notch signaling: the core pathway and its posttranslational regulationDev Cell2009 16633647
Not in our library10.1016/j.devcel.2009.03.010
184.
Ho IC Hodge MR Rooney JW Glimcher LH The proto-oncogene c-maf is responsible for tissue-specific expression of interleukin-4Cell1996 85973983
Not in our library10.1016/s0092-8674(00)81299-4
185.
Ho IC Lo D Glimcher LH c-maf promotes T helper cell type 2 (Th2) and attenuates Th1 differentiation by both interleukin 4-dependent and -independent mechanismsJ Exp Med1998 18818591866
Not in our library10.1084/jem.188.10.1859
186.
Ko E Rho S Cho C Choi H Ko S Lee Y Hong MC Shin MK Jung SG Bae H So-Cheong-Ryong-Tang, tradititional Korean medicine, suppresses Th2 lineage developmentBiol Pharm Bull2004 27739743
Not in our library10.1248/bpb.27.739
187.
Won HY Min HJ Ahn JH Yoo SE Bae MA Hong JH Hwang ES Anti-allergic function and regulatory mechanisms of KR62980 in allergen-induced airway inflammationBiochem Pharmacol2009
Not in our library10.1016/j.bcp.2009.10.023
188.
Liu Z Li Z Mao K Zou J Wang Y Tao Z Lin G Tian L Ji Y Wu X Dec2 promotes Th2 cell differentiation by enhancing IL-2R signalingJ Immunol2009 18363206329
Not in our library10.4049/jimmunol.0900975
189.
Yang XO Angkasekwinai P Zhu J Peng J Liu Z Nurieva R Liu X Chung Y Chang SH Sun B Dong C Requirement for the basic helix-loop-helix transcription factor Dec2 in initial TH2 lineage commitmentNat Immunol2009 1012601266
Not in our library10.1038/ni.1821
190.
Shinnakasu R Yamashita M Kuwahara M Hosokawa H Hasegawa A Motohashi S Nakayama T Gfi1-mediated stabilization of GATA3 protein is required for Th2 cell differentiationJ Biol Chem2008 2832821628225
Not in our library10.1074/jbc.m804174200
191.
Hirahara K Yamashita M Iwamura C Shinoda K Hasegawa A Yoshizawa H Koseki H Gejyo F Nakayama T Repressor of GATA regulates TH2-driven allergic airway inflammation and airway hyperresponsivenessJ Allergy Clin Immunol2008 122512520e511
Not in our library10.1016/j.jaci.2008.06.004
192.
Kusam S Toney LM Sato H Dent AL Inhibition of Th2 differentiation and GATA-3 expression by BCL-6J Immunol2003 17024352441
Not in our library10.4049/jimmunol.170.5.2435
193.
Yoshimura A Naka T Kubo M SOCS proteins, cytokine signalling and immune regulationNat Rev Immunol2007 7454465
Not in our library10.1038/nri2093
194.
Seki Y Inoue H Nagata N Hayashi K Fukuyama S Matsumoto K Komine O Hamano S Himeno K Inagaki-Ohara K SOCS-3 regulates onset and maintenance of T(H)2-mediated allergic responsesNat Med2003 910471054
Not in our library10.1038/nm896
195.
Taleb S Romain M Ramkhelawon B Uyttenhove C Pasterkamp G Herbin O Esposito B Perez N Yasukawa H Van Snick J Loss of SOCS3 expression in T cells reveals a regulatory role for interleukin-17 in atherosclerosisJ Exp Med2009 20620672077
Not in our library10.1084/jem.20090545
196.
Seki Y Hayashi K Matsumoto A Seki N Tsukada J Ransom J Naka T Kishimoto T Yoshimura A Kubo M Expression of the suppressor of cytokine signaling-5 (SOCS5) negatively regulates IL-4-dependent STAT6 activation and Th2 differentiationProc Natl Acad Sci USA2002 991300313008
Not in our library10.1073/pnas.202477099
197.
Ohshima M Yokoyama A Ohnishi H Hamada H Kohno N Higaki J Naka T Overexpression of suppressor of cytokine signalling-5 augments eosinophilic airway inflammation in miceClin Exp Allergy2007 37735742
Not in our library10.1111/j.1365-2222.2007.02707.x
198.
Lu TX Munitz A Rothenberg ME MicroRNA-21 is up-regulated in allergic airway inflammation and regulates IL-12p35 expressionJ Immunol2009 18249945002
Not in our library10.4049/jimmunol.0803560
199.
Mattes J Collison A Plank M Phipps S Foster PS Antagonism of microRNA-126 suppresses the effector function of TH2 cells and the development of allergic airways diseaseProc Natl Acad Sci USA2009 1061870418709
Not in our library10.1073/pnas.0905063106
200.
Hur GY Lee SY Lee SH Kim SJ Lee KJ Jung JY Lee EJ Kang EH Jung KH Kim JH Potential use of an anticancer drug gefinitib, an EGFR inhibitor, on allergic airway inflammationExp Mol Med2007 39367375
Not in our library10.1038/emm.2007.41
201.
Yamamoto N Takeshita K Shichijo M Kokubo T Sato M Nakashima K Ishimori M Nagai H Li YF Yura T Bacon KB The orally available spleen tyrosine kinase inhibitor 2-[7-(3,4-dimethoxyphenyl)-imidazo[1,2-c]pyrimidin-5-ylamino]nicotinamide dihydrochloride (BAY 61-3606) blocks antigen-induced airway inflammation in rodentsJ Pharmacol Exp Ther2003 30611741181
Not in our library10.1124/jpet.103.052316
202.
Meltzer EO Berkowitz RB Grossbard EB An intranasal Syk-kinase inhibitor (R112) improves the symptoms of seasonal allergic rhinitis in a park environmentJ Allergy Clin Immunol2005 115791796
Not in our library10.1016/j.jaci.2005.01.040
203.
Kudlacz E Conklyn M Andresen C Whitney-Pickett C Changelian P The JAK-3 inhibitor CP-690550 is a potent anti-inflammatory agent in a murine model of pulmonary eosinophiliaEur J Pharmacol2008 582154161
Not in our library10.1016/j.ejphar.2007.12.024
204.
Malaviya R Chen CL Navara C Liu XP Keenan M Waurzyniak B Uckun FM Treatment of allergic asthma by targeting janus kinase 3-dependent leukotriene synthesis in mast cells with 4-(3', 5'-dibromo-4'-hydroxyphenyl)amino-6,7-dimethoxyquinazoline (WHI-P97)J Pharmacol Exp Ther2000 295912926
Not in our library
205.
Malaviya R Zhu D Dibirdik I Uckun FM Targeting Janus kinase 3 in mast cells prevents immediate hypersensitivity reactions and anaphylaxisJ Biol Chem1999 2742702827038
Not in our library10.1074/jbc.274.38.27028
206.
Duan W Chan JH Wong CH Leung BP Wong WS Anti-inflammatory effects of mitogen-activated protein kinase kinase inhibitor U0126 in an asthma mouse modelJ Immunol2004 17270537059
Not in our library10.4049/jimmunol.172.11.7053
207.
Duan W Chan JH McKay K Crosby JR Choo HH Leung BP Karras JG Wong WS Inhaled p38 alpha mitogen-activated protein kinase antisense oligonucleotide attenuates asthma in miceAm J Respir Crit Care Med2005 171571578
Not in our library10.1164/rccm.200408-1006oc
208.
Adcock IM Chung KF Caramori G Ito K Kinase inhibitors and airway inflammationEur J Pharmacol2006 533118132
Not in our library10.1016/j.ejphar.2005.12.054
209.
Barnes PJ Novel signal transduction modulators for the treatment of airway diseasesPharmacol Ther2006 109238245
Not in our library10.1016/j.pharmthera.2005.08.001
210.
Gruenbaum LM Schwartz R Woska JR Jr DeLeon RP Peet GW Warren TC Capolino A Mara L Morelock MM Shrutkowski A Inhibition of pro-inflammatory cytokine production by the dual p38/JNK2 inhibitor BIRB796 correlates with the inhibition of p38 signalingBiochem Pharmacol2009 77422432
Not in our library10.1016/j.bcp.2008.10.032
211.
Chialda L Zhang M Brune K Pahl A Inhibitors of mitogen-activated protein kinases differentially regulate costimulated T cell cytokine production and mouse airway eosinophiliaRespir Res2005 636
Not in our library10.1186/1465-9921-6-36
212.
Nath P Eynott P Leung SY Adcock IM Bennett BL Chung KF Potential role of c-Jun NH2-terminal kinase in allergic airway inflammation and remodelling: effects of SP600125Eur J Pharmacol2005 506273283
Not in our library10.1016/j.ejphar.2004.11.040
213.
Trifilieff A Keller TH Press NJ Howe T Gedeck P Beer D Walker C CGH2466, a combined adenosine receptor antagonist, p38 mitogen-activated protein kinase and phosphodiesterase type 4 inhibitor with potent in vitro and in vivo anti-inflammatory activitiesBr J Pharmacol2005 14410021010
Not in our library10.1038/sj.bjp.0706132
214.
Lee KS Park SJ Kim SR Min KH Lee KY Choe YH Hong SH Lee YR Kim JS Hong SJ Lee YC Inhibition of VEGF blocks TGF-beta1 production through a PI3K/Akt signalling pathwayEur Respir J2008 31523531
Not in our library10.1183/09031936.00125007
215.
Park SJ Min KH Lee YC Phosphoinositide 3-kinase delta inhibitor as a novel therapeutic agent in asthmaRespirology2008 13764771
Not in our library10.1111/j.1440-1843.2008.01369.x
216.
Birrell MA Hardaker E Wong S McCluskie K Catley M De Alba J Newton R Haj-Yahia S Pun KT Watts CJ Ikappa-B kinase-2 inhibitor blocks inflammation in human airway smooth muscle and a rat model of asthmaAm J Respir Crit Care Med2005 172962971
Not in our library10.1164/rccm.200412-1647oc
217.
Ziegelbauer K Gantner F Lukacs NW Berlin A Fuchikami K Niki T Sakai K Inbe H Takeshita K Ishimori M A selective novel low-molecular-weight inhibitor of IkappaB kinase-beta (IKK-beta) prevents pulmonary inflammation and shows broad anti-inflammatory activityBr J Pharmacol2005 145178192
Not in our library10.1038/sj.bjp.0706176
218.
Hirose K Wakashin H Oki M Kagami S Suto A Ikeda K Watanabe N Iwamoto I Furuichi Y Nakajima H GS143, an IkappaB ubiquitination inhibitor, inhibits allergic airway inflammation in miceBiochem Biophys Res Commun2008 374507511
Not in our library10.1016/j.bbrc.2008.07.072
219.
Lu S Liu N Dass SB Reiss TF Knorr BA Randomized, placebo-controlled study of a selective PDE4 inhibitor in the treatment of asthmaRespir Med2009 103342347
Not in our library10.1016/j.rmed.2008.10.024
220.
Singh D Petavy F Macdonald AJ Lazaar AL O'Connor BJ The inhaled phosphodiesterase 4 inhibitor GSK256066 reduces allergen challenge responses in asthmaRespir Res2010 1126
Not in our library10.1186/1465-9921-11-26
221.
Boswell-Smith V Spina D Oxford AW Comer MB Seeds EA Page CP The pharmacology of two novel long-acting phosphodiesterase 3/4 inhibitors, RPL554 [9,10-dimethoxy-2(2,4,6-trimethylphenylimino)-3-(n-carbamoyl-2-aminoethyl) -3,4,6,7-tetrahydro-2H-pyrimido[6,1-a]isoquinolin-4-one] and RPL565 [6,7-dihydro-2-(2,6-diisopropylphenoxy)-9,10-dimethoxy-4H-pyrimido[6,1-a]i soquinolin-4-one]J Pharmacol Exp Ther2006 318840848
Not in our library10.1124/jpet.105.099192
222.
Hoyer KK Dooms H Barron L Abbas AK Interleukin-2 in the development and control of inflammatory diseaseImmunol Rev2008 2261928
Not in our library10.1111/j.1600-065x.2008.00697.x
223.
Rothenberg ME Owen WF Jr Silberstein DS Woods J Soberman RJ Austen KF Stevens RL Human eosinophils have prolonged survival, enhanced functional properties, and become hypodense when exposed to human interleukin 3The Journal of clinical investigation1988 8119861992
Not in our library10.1172/jci113547
224.
Valent P Dahinden CA Role of interleukins in the regulation of basophil development and secretionCurrent opinion in hematology2010 176066
Not in our library10.1097/moh.0b013e328331fae9
225.
Asquith KL Ramshaw HS Hansbro PM Beagley KW Lopez AF Foster PS The IL-3/IL-5/GM-CSF common receptor plays a pivotal role in the regulation of Th2 immunity and allergic airway inflammationJ Immunol2008 18011991206
Not in our library10.4049/jimmunol.180.2.1199
226.
Webb DC Cai Y Matthaei KI Foster PS Comparative roles of IL-4, IL-13, and IL-4Ralpha in dendritic cell maturation and CD4+ Th2 cell functionJ Immunol2007 178219227
Not in our library10.4049/jimmunol.178.1.219
227.
Corren J Busse W Meltzer EO Mansfield L Bensch G Fahrenholz J Wenzel SE Chon Y Dunn M Weng HH Lin SL A randomized, controlled, phase 2 study of AMG 317, an IL-4Ralpha antagonist, in patients with asthmaAmerican journal of respiratory and critical care medicine2010 181788796
Not in our library10.1164/rccm.200909-1448oc
228.
Wenzel S Wilbraham D Fuller R Getz EB Longphre M Effect of an interleukin-4 variant on late phase asthmatic response to allergen challenge in asthmatic patients: results of two phase 2a studiesLancet2007 37014221431
Not in our library10.1016/s0140-6736(07)61600-6
229.
Oh CK Geba GP Molfino N Investigational therapeutics targeting the IL-4/IL-13/STAT-6 pathway for the treatment of asthmaEuropean respiratory review: an official journal of the European Respiratory Society2010 194654
Not in our library10.1183/09059180.00007609
230.
Leckie MJ Anti-interleukin-5 monoclonal antibodies: preclinical and clinical evidence in asthma modelsAm J Respir Med2003 2245259
Not in our library10.1007/bf03256653
231.
Leckie MJ ten Brinke A Khan J Diamant Z O'Connor BJ Walls CM Mathur AK Cowley HC Chung KF Djukanovic R Effects of an interleukin-5 blocking monoclonal antibody on eosinophils, airway hyper-responsiveness, and the late asthmatic responseLancet2000 35621442148
Not in our library10.1016/s0140-6736(00)03496-6
232.
Busse WW Katial R Gossage D Sari S Wang B Kolbeck R Coyle AJ Koike M Spitalny GL Kiener PA Safety profile, pharmacokinetics, and biologic activity of MEDI-563, an anti-IL-5 receptor alpha antibody, in a phase I study of subjects with mild asthmaJ Allergy Clin Immunol2010 12512371244e1232
Not in our library10.1016/j.jaci.2010.04.005
233.
Haldar P Brightling CE Hargadon B Gupta S Monteiro W Sousa A Marshall RP Bradding P Green RH Wardlaw AJ Pavord ID Mepolizumab and exacerbations of refractory eosinophilic asthmaThe New England journal of medicine2009 360973984
Not in our library10.1056/nejmoa0808991
234.
Nair P Pizzichini MM Kjarsgaard M Inman MD Efthimiadis A Pizzichini E Hargreave FE O'Byrne PM Mepolizumab for prednisone-dependent asthma with sputum eosinophiliaN Engl J Med2009 360985993
Not in our library10.1056/nejmoa0805435
235.
Rincon M Anguita J Nakamura T Fikrig E Flavell RA Interleukin (IL)-6 directs the differentiation of IL-4-producing CD4+ T cellsJ Exp Med1997 185461469
Not in our library10.1084/jem.185.3.461
236.
Mucida D Salek-Ardakani S Regulation of TH17 cells in the mucosal surfacesJ Allergy Clin Immunol2009 1239971003
Not in our library10.1016/j.jaci.2009.03.016
237.
Weissenbach M Clahsen T Weber C Spitzer D Wirth D Vestweber D Heinrich PC Schaper F Interleukin-6 is a direct mediator of T cell migrationEur J Immunol2004 3428952906
Not in our library10.1002/eji.200425237
238.
Renauld JC Goethals A Houssiau F Merz H Van Roost E Van Snick J Human P40/IL-9. Expression in activated CD4+ T cells, genomic organization, and comparison with the mouse geneJ Immunol1990 14442354241
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239.
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240.
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241.
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Not in our library10.1016/j.clinthera.2009.04.019
242.
Safety profile and clinical activity of multiple subcutaneous doses of MEDI-528, a humanized anti-interleukin-9 monoclonal antibody, in two randomized phase 2a studies in subjects with asthma · 2011
Not checked
243.
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Not in our library10.1111/j.1600-065x.2008.00635.x
244.
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245.
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246.
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247.
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248.
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Not in our library10.1111/j.1365-2222.2009.03383.x
249.
Kasaian MT Miller DK IL-13 as a therapeutic target for respiratory diseaseBiochem Pharmacol2008 76147155
Not in our library10.1016/j.bcp.2008.04.002
250.
Ishimitsu R Nishimura H Yajima T Watase T Kawauchi H Yoshikai Y Overexpression of IL-15 in vivo enhances Tc1 response, which inhibits allergic inflammation in a murine model of asthmaJ Immunol2001 16619912001
Not in our library10.4049/jimmunol.166.3.1991
251.
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Not in our library10.1165/rcmb.4832
252.
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Not in our library10.1084/jem.20061401
253.
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Not in our library10.1146/annurev.immunol.19.1.423
254.
Maecker HT Hansen G Walter DM DeKruyff RH Levy S Umetsu DT Vaccination with allergen-IL-18 fusion DNA protects against, and reverses established, airway hyperreactivity in a murine asthma modelJ Immunol2001 166959965
Not in our library10.4049/jimmunol.166.2.959
255.
Huang F Wachi S Thai P Loukoianov A Tan KH Forteza RM Wu R Potentiation of IL-19 expression in airway epithelia by IL-17A and IL-4/IL-13: important implications in asthmaJ Allergy Clin Immunol2008 12114151421
Not in our library10.1016/j.jaci.2008.04.016
256.
Liao SC Cheng YC Wang YC Wang CW Yang SM Yu CK Shieh CC Cheng KC Lee MF Chiang SR IL-19 induced Th2 cytokines and was up-regulated in asthma patientsJ Immunol2004 17367126718
Not in our library10.4049/jimmunol.173.11.6712
257.
Sivakumar PV Foster DC Clegg CH Interleukin-21 is a T-helper cytokine that regulates humoral immunity and cell-mediated anti-tumour responsesImmunology2004 112177182
Not in our library10.1111/j.1365-2567.2004.01886.x
258.
Besnard AG Sabat R Dumoutier L Renauld JC Willart M Lambrecht B Teixeira MM Charron S Fick L Erard F Dual Role of IL-22 in allergic airway inflammation and its cross-talk with IL-17AAm J Respir Crit Care Med2011 18311531163
Not in our library10.1164/rccm.201008-1383oc
259.
Wakashin H Hirose K Maezawa Y Kagami S Suto A Watanabe N Saito Y Hatano M Tokuhisa T Iwakura Y IL-23 and Th17 cells enhance Th2-cell-mediated eosinophilic airway inflammation in miceAm J Respir Crit Care Med2008 17810231032
Not in our library10.1164/rccm.200801-086oc
260.
Li Y Sun M Cheng H Li S Liu L Qiao H Hua S Lu J Silencing IL-23 expression by a small hairpin RNA protects against asthma in miceExp Mol Med2011 43197204
Not in our library10.3858/emm.2011.43.4.024
261.
Ballantyne SJ Barlow JL Jolin HE Nath P Williams AS Chung KF Sturton G Wong SH McKenzie AN Blocking IL-25 prevents airway hyperresponsiveness in allergic asthmaJ Allergy Clin Immunol2007 12013241331
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262.
Wang YH Angkasekwinai P Lu N Voo KS Arima K Hanabuchi S Hippe A Corrigan CJ Dong C Homey B IL-25 augments type 2 immune responses by enhancing the expansion and functions of TSLP-DC-activated Th2 memory cellsJ Exp Med2007 20418371847
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263.
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Not in our library10.4049/jimmunol.179.7.4415
264.
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Not in our library10.1038/ni1084
265.
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266.
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267.
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268.
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Not in our library10.1016/j.immuni.2005.09.015
269.
Shannon J Ernst P Yamauchi Y Olivenstein R Lemiere C Foley S Cicora L Ludwig M Hamid Q Martin JG Differences in airway cytokine profile in severe asthma compared to moderate asthmaChest2008 133420426
Not in our library10.1378/chest.07-1881
270.
Yang M Kumar RK Foster PS Pathogenesis of steroid-resistant airway hyperresponsiveness: interaction between IFN-gamma and TLR4/MyD88 pathwaysJ Immunol2009 18251075115
Not in our library10.4049/jimmunol.0803468
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Boguniewicz M Schneider LC Milgrom H Newell D Kelly N Tam P Izu AE Jaffe HS Bucalo LR Leung DY Treatment of steroid-dependent asthma with recombinant interferon-gammaClin Exp Allergy1993 23785790
Not in our library10.1111/j.1365-2222.1993.tb00367.x
272.
Gorelik L Fields PE Flavell RA Cutting edge: TGF-beta inhibits Th type 2 development through inhibition of GATA-3 expressionJ Immunol2000 16547734777
Not in our library10.4049/jimmunol.165.9.4773
273.
Fattouh R Midence NG Arias K Johnson JR Walker TD Goncharova S Souza KP Gregory RC Jr Lonning S Gauldie J Jordana M Transforming growth factor-beta regulates house dust mite-induced allergic airway inflammation but not airway remodelingAm J Respir Crit Care Med2008 177593603
Not in our library10.1164/rccm.200706-958oc
274.
Alcorn JF Rinaldi LM Jaffe EF van Loon M Bates JH Janssen-Heininger YM Irvin CG Transforming growth factor-beta1 suppresses airway hyperresponsiveness in allergic airway diseaseAm J Respir Crit Care Med2007 176974982
Not in our library10.1164/rccm.200702-334oc
275.
Brightling C Berry M Amrani Y Targeting TNF-alpha: a novel therapeutic approach for asthmaJ Allergy Clin Immunol2008 121510quiz 11-12
Not in our library10.1016/j.jaci.2007.10.028
276.
Berry MA Pavord ID Antagonism of tumour necrosis factor alpha in refractory asthmaThorax2008 63571572
Not in our library10.1136/thx.2007.095042
277.
Wenzel SE Barnes PJ Bleecker ER Bousquet J Busse W Dahlen SE Holgate ST Meyers DA Rabe KF Antczak A A randomized, double-blind, placebo-controlled study of tumor necrosis factor-alpha blockade in severe persistent asthmaAm J Respir Crit Care Med2009 179549558
Not in our library10.1164/rccm.200809-1512oc

Cited by papers we hold 2

1'-Acetoxychavicol acetate isolated from Alpinia galanga ameliorates ovalbumin-induced asthma in mice. · 2013
Not checked
Mesenchymal Stem Cells in Tissue Repair · 2013
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