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Glucocorticoids, Sex Hormones, and Immunity

Oxana Bereshchenko, Stefano Bruscoli, Carlo Riccardi

Frontiers in Immunology · 2018 · Review

doi:10.3389/fimmu.2018.01332

Abstract

Glucocorticoid hormones regulate essential body functions in mammals, control cell metabolism, growth, differentiation, and apoptosis. Importantly, they are potent suppressors of inflammation, and multiple immune-modulatory mechanisms involving leukocyte apoptosis, differentiation, and cytokine production have been described. Due to their potent anti-inflammatory and immune-suppressive activity, synthetic glucocorticoids (GCs) are the most prescribed drugs used for treatment of autoimmune and inflammatory diseases. It is long been noted that males and females exhibit differences in the prevalence in several autoimmune diseases (AD). This can be due to the role of sexual hormones in regulation of the immune responses, acting through their endogenous nuclear receptors to mediate gene expression and generate unique gender-specific cellular environments. Given the fact that GCs are the primary physiological anti-inflammatory hormones, and that sex hormones may also exert immune-modulatory functions, the link between GCs and sex hormones may exist. Understanding the nature of this possible crosstalk is important to unravel the reason of sexual disparity in AD and to carefully prescribe these drugs for the treatment of inflammatory diseases. In this review, we discuss similarities and differences between the effects of sex hormones and GCs on the immune system, to highlight possible axes of functional interaction.

Full text

From PubMed Central, U.S. National Library of Medicine, as current on Oct 20, 2026. Paragraph numbers are ours, so an answer can point at one.

Introduction

The interaction between endocrine and immune systems ensures the correct function of immune system. Women mount stronger immune responses against foreign but also against self-antigens, and the prevalence of most autoimmune diseases (AD) is greatly increased in women compared to men. An important role underlying the difference in activity of immune cells in men and women is attributed to sex hormones.

Steroid hormones, such as estrogens, prolactin, progesterone, and glucocorticoids (GCs) modulate the development and activity of both innate and adaptive immunity differently in men and women. Therefore, characterization of the mechanisms of hormonal regulation of different immune cell types is important for understanding the regulatory circuits critical for keeping a competent and a healthy immune system and to improve therapy of AD.

The degree and the duration of the immune response is influenced by the number and the type of circulating immune cells; therefore, the effect of steroid hormones on survival and differentiation of T and B lymphocytes and cells of innate immune system will define the numeric leukocyte output in the periphery. Hormonal regulation of cytokine production impacts on differentiation of naïve T cells into the particular effector subtypes, thus defining the type of the mounted immune responses. Interestingly, since sex hormones and GCs are acting on the same cellular pathways that regulate leukocytes growth, differentiation, and survival, their simultaneous action would likely enhance or abrogate the effects elicited by individual factors. Therefore, biologic differences in endogenous GCs levels, as well as exposure of an individual to specific environmental stimuli, including presence of chronic inflammatory disease, prolonged stress, metabolic challenges or injuries, as well as pharmacologic administration of exogenous GCs, will alter the expected gender-related effects on immunity and ADs. The converging and diverging effects of GCs and sex hormones on different cells types of the immune system are discussed in this minireview.

Steroid Hormones: Mechanisms of Action

Corticosteroids and sex hormones are derived from cholesterol through the same sterodoigenic pathway, with common metabolic intermediate, progesterone, and are under the control of the hypothalamus–pituitary–adrenal gland (HPA) axis. The main natural GCs (i.e., cortisol) are produced in the cortical part of the adrenal gland. Biosynthesis of androgens, including testosterone, occurs mainly in Leydig cells in male gonads, and small amounts are produced by the ovary and adrenal cortex in females. The androgens dehydroepiandrosterone (DHEA), androstenedione, and testosterone are the precursors of estrogens, produced in females primarily in ovaries.

Glucocorticoids

Glucocorticoids are essential endocrine regulators of body functions in homeostasis and adaptation to environmental changes. One important feature of GCs regulation is the circadian control of GCs secretion by the HPA axis. The rhythmically released GCs may have an impact on immunity regulation. Endogenous GCs act on a variety of cell types to regulate the expression of genes controlling cellular metabolism, growth, differentiation, and apoptosis. Thus, proper production and activity of the endogenous GCs is critical for the regulation of inflammatory events during tissue repair and pathogens elimination. Due to their potent immune-suppressive and anti-inflammatory function, synthetic GCs are extensively used in clinic to treat acute and chronic inflammation.

The GCs act via genomic (transcriptional) and non-genomic (transcription-independent) mechanisms. Most cellular actions of GCs are mediated by binding to its cognate intracellular receptor (GR), transcription factor of the nuclear receptors (NR) superfamily. GR shares functional domains with other NR that include an N-terminal transactivation domain, a highly conserved central DNA binding domain, and a C-terminal ligand-binding domain. After ligand-induced conformational changes, GR translocates into the nucleus where it regulates transcription of hundreds of genes. It may bind directly to DNA via glucocorticoid recognition elements, or regulate gene expression via indirect mechanisms. GR may directly interact with NF-κB, a key transcription factor that activates many pro-inflammatory genes, as well as with other transcription factors (TFs), such as STAT-3 and -5, AP-1, and CREB. GR does not interfere with the DNA binding activity of NF-κB, but inhibits its transcriptional activation function via preventing its nuclear translocation, or interfering with transcriptional machinery by competition with co-factors such as p300/CBP, thus repressing the expression of pro-inflammatory genes, such as TNF-α, IL-1, and ICAM-1. Mechanisms of GCs actions also include induction of proteins with anti-inflammatory activities, such as glucocorticoid-induced leucine zipper (GILZ), which mediates many of the GCs’ activities, including inhibition of RAS/RAF/MAPK pathways, and of NF-κB and AP-1 activities. “Non-genomic” effects of GCs include direct interaction of liganded GR with diverse intracellular mediators and modulating several signaling pathways, including protein kinase C, phosphatidylinositol-specific phospholipase C, and src kinase pathways.

Sex Hormones

Sex hormones regulate reproductive and metabolic body functions throughout the life of the subjects. Sex hormones influence immune cell function and inflammation: androgens are mainly anti-inflammatory, whereas estrogens have both pro- and anti-inflammatory roles, depending on several factors, such as type of immune response or variability of expression of different estrogen receptor (ER) isoforms.

Estrogens exert their effects through binding to ERα or ERβ, TFs of NR superfamily that regulate expression of genes involved in cell survival, proliferation, differentiation, and reproductive functions. Similar to GR, nuclear ERs bind DNA either directly through estrogen response elements, or indirectly, via ERE-independent TFs, such as NF-κB, SP1, AP-1, C/EBPβ, to induce or repress gene expression. Estrogens also elicit rapid (“non-genomic”) signal transduction effects, via modulation of intracellular calcium, cAMP, potassium currents, phospholipase C activation, and stimulation of PI3K/AKT and ERK pathways.

Estrogen receptors are expressed in various types of immune cells, including lymphocytes, macrophages, and dendritic cells (DC). Estrogens were shown to exert both, anti- and pro-inflammatory effects, depending on the context and combination of factors that include: the type of the immune cell target, the concentration of the hormone, the type of immune stimulus (foreign or auto-antigens), the target organ microenvironment, and the relative expression of ERα and ERβ. Estrogens may promote inflammation via regulation of the expression of inflammatory mediators via Akt/mTOR pathway. However, pregnancy or higher doses of ectopic estrogens typically suppress immune responses, by repressing the expression of multiple NF-κB- and c-Jun-driven cytokine genes, similar to GCs. ERα may displace p65 and CREB and their associated co-regulators from NF-κB binding site. Progesterone (P4) is produced at high levels during the menstrual cycle and during pregnancy. P4 signals through the progesterone receptor (PR) and to a lesser extent, through GR and mineralocorticoid receptors. P4 is expressed in different immune cells types, including NK, macrophages, DCs, and T cells, and have broad anti-inflammatory effects of the immune system by decreasing leukocytes activation and production of pro-inflammatory mediators. NF-κB inhibition is also suggested to play a role in these effects of P4.

Similar to GCs, male steroid hormones demonstrate mostly the suppressive role in immune function, via binding to androgen receptor (AR), also a member of NR superfamily, and regulation of target gene expression. AR recognizes directly the androgen response elements in the regulatory regions of AR target genes. Androgens, including dihydrotestosterone and testosterone, generally suppress immune cell activity, by reducing the inflammatory and promoting anti-inflammatory mediators’ expression by macrophages and T cells. The levels of androgen DHEA are reduced in patients with RA and inflammatory bowel disease suggesting that DHEA may cover many aspects of immune regulatory effects of sex hormones.

Moreover, an indirect immunomodulatory effect of androgens may be related to the anti-inflammatory activity of endogenous GCs due to their effect on the HPA axis.

Effect of Steroid Hormones on Innate Immunity

Both GCs and sex steroid modulate the development and function of various cells of innate immunity, including neutrophils, macrophages, natural killer cells, and DC (Table 1). GCs actions include regulation of apoptosis in many cell types: they exert a protective effect in macrophages, by inhibiting activation of caspases and contributing to inflammation resolution; however, prolonged usage of GCs promotes apoptosis in macrophages, natural killer cells, DC, neutrophils, and eosinophils. To the contrary, estrogens and androgens increase the number of neutrophils.

Glucocorticoids have mainly suppressive effects on the cells of innate immunity (Table 1). High doses of GCs inhibit most of the functions of tissue macrophages, such as chemotaxis, phagocytosis, proliferation, and antigen presentation. GCs suppress the expression of various pro-inflammatory cytokines released by macrophages, such as IFN-γ, IL-1α, and IL-1β. In addition, the synthesis of anti-inflammatory molecules annexin A1 and GILZ in macrophages contributes to the anti-inflammatory and immunosuppressive action of GCs. GCs also inhibit monocytes’ chemotaxis by reducing expression of chemokines, such as CXCL-1, IL-8 and CXCL-2, and CCL2, control granulocyte trafficking by reducing expression of adhesion molecules, such as Mac-1 and L-selectin on neutrophils, thus limiting the inflammatory response. In addition, GCs prevent neutrophils migration into inflamed tissues via the upregulation of GILZ and annexin A1. Similar to GCs, treatment with estrogens inhibits neutrophils’ activity by restricting their recruitment and inhibiting the NFκB-dependent production of major neutrophil chemoattractants CXCL-1, CXCL2, CXCL3, and CXCL8 in experimental models of tissue injury. Estradiol inhibits neutrophil activation through a reduction in oxidative metabolism, adhesion to endothelial cells via upregulation of the anti-inflammatory protein annexin A1, and attenuates the release of pro-inflammatory cytokines, such as TNF-α, IL-1β, and IL-6 in human peripheral blood mononuclear cells and in neutrophils and macrophages. Interestingly, the inhibition of NFκB activity is a central mechanism underlying these actions.

Glucocorticoids and estrogens have both convergent and divergent actions in DCs. GCs inhibit DC function in several ways: by promoting apoptosis, disturbing maturation of immature DCs, and inducing a tolerogenic phenotype, via downregulating the expression of major histocompatibility complex (MHC)-II and co-stimulatory molecules and cytokines, such as IL-1, IL-6, and IL-12. Such changes are associated with reduced proliferative and T helper 1 (Th1) responses by T cells, and increase in immunosuppressive regulatory T (Treg) cells. Instead, estrogens promote DC cell differentiation and MHCII expression, and induce the expression of IL-6, IL-23, IL-12, and IL-1β, thus increasing the type-1 responses. On the other hand, similar to GCs, estrogens induce a tolerogenic phenotype in DC, by decreasing the expression of pro-inflammatory cytokines and chemokines, such as IL-6, IFN-γ, IL-12, CXCL8, and CCL2, and upregulating inhibitory molecules PD-L1 and PD-L2, and regulatory cytokines IL-10 and TGF-β, thus also leading to a decrease in the Th1 cells activation and a shift toward production of Th2-type cytokines.

Effect of Steroid Hormones on Adaptive Immunity

Controlled elimination of T cells during thymocyte development and T cell-mediated immune responses is essential to prevent immunopathologies, such as autoimmunity and cancer. GCs induce apoptosis in developing thymocytes and regulate both “death by neglect” and positive selection. The GC-induced apoptosis in thymocytes is also attributed to non-genomic effects of GR. Their role in positive selection is inferred from the antagonism between GCs and T cell repertoire (TCR)-activated signals, which allows cells with intermediate TCR affinity to be positively selected.

The growth suppressive effect of GCs on thymocytes is common to the action of female and male sex hormones. Similar to GCs, estrogens inhibit thymocyte proliferation and induce thymic atrophy. Pregnancy is associated with accelerated thymic involution. Androgens also restrain active cell cycling and the number of immature thymocytes. The number of CD4+ and CD8+ T cells is lower in males around 50–75 of age compared to females, and the diversity of the TCR in females is larger than in males of the same age.

Upon TCR activation and stimulation with particular cytokines, naïve mature CD4+ T cells differentiate in the periphery into one of several lineages of T helper (Th) cells that include Th1, Th2, Th17, and Treg cells. GCs promote the shift from Th1 to Th2 type immune responses by differentially regulating apoptosis of Th1 and Th2 cells, and by interfering with the activity of their master regulators T-bet and GATA-3, respectively. GCs can also suppress the production of TNF-α, IL-12, and IFN-γ and induce the production of IL-4, IL-10, and IL-13. GCs inhibit the production of Th17-type cytokines in AD, although the sensitivity of Th17 cells to GC-induced apoptosis varies dependent on disease-specific microenvironment. Treg cells play a critical role in regulating immune responses and peripheral tolerance. GCs upregulate expression of FoxP3, the master regulator of Treg cells, expand Treg cell population, and increase Treg function in AD. Expression of GCs’ target gene GILZ also contributes to the GC-mediated regulation of Th1/Th2 balance, and the induction of Treg cells by promoting TGF-β-dependent FoxP3 expression.

Sex steroids also modulate the differentiation and function of all subsets of T cells. Contrary to GCs, estrogens promote INF-γ production by Th1 cells in both human and mice, via potentially direct interaction of ER with the Ifng promoter, upregulation of Th-1 transcription factor T-bet, or via microRNA-dependent suppression of IFN-γ expression. However, high levels of estrogen skew the immune response from Th1 to Th2-type, similar to GCs. Estradiol also regulates anti-inflammatory Th2 shift by activating SGK1 kinase. The effects of estrogens on Th17 subset are different depending on experimental model, leading to enhancement or decrease of Th17-dependent inflammation. Like GCs, estrogens promote the expansion of Treg cells by upregulating the expression of FoxP3, PD-1, and CTLA-4, therefore, GCs and estrogens may co-operate in promoting the Treg development and activity.

Glucocorticoids and estrogens elicit opposite effects on B cells. GCs have a pro-apoptotic effect on developing B lymphocytes in the bone marrow. On the other hand, B-lymphoblastic leukemia cells are resistant to GC-induced apoptosis, due to enhanced expression of B-cell lymphoma-2 protein. GILZ mediates GC-induced apoptosis in B cells as shown by the accumulation of B cells in the bone marrow and in the periphery in GILZ-deficient mice, due to reduced B cell apoptosis. GCs affect directly humoral response by reducing circulating immunoglobulins (Igs) although some studies have shown an increase of IgE production in conjunction with IL-4. Instead, enhanced antibody production is observed in women, suggesting that female sex hormones stimulate B cell-mediated responses. Estrogen treatment also interferes with normal tolerance of naive DNA-reactive B cells, thus contributing to the development of AD. Elevated estrogen alters the negative selection of DNA-reactive B cells in the periphery, interfering with proper B cell receptor signaling and regulation of B cells activation and apoptosis. Thus, pharmacologic treatment with synthetic GCs may be useful in suppression of the enhanced B cell activities in AD.

Effect of Steroid Hormones on Innate Lymphoid Cells (ILC)

Innate lymphoid cell is a most recently identified immune cell type, which contributes to inflammation, immunity, and the maintenance of tissue integrity and homeostasis. Recent evidence demonstrated that group 2 ILC2s are present in the uterus under control of estrogens and are increased upon estrogen administration. It is, therefore, possible that estrogens modulate tolerance via ILC2-mediated modulation of the protective Th2 shift in pregnancy. Instead, ILC2 promote lung inflammation during asthma. Interestingly, male mice have reduced numbers of ILC2s in peripheral tissues compared to females, and the number of ILC2s in the lungs is negatively regulated by androgens, consistent with the overall suppressive role of male steroids in immunity. GCs were shown to modulate the cytokine production by the ILC2s, thus these finding suggests a modulatory role of steroid hormones in ILCs and homeostasis of specific tissues.

Interaction Between GR and Sex Hormone Receptors

GR, ER, and AR are ligand-activated TFs belonging to the NR superfamily. Experimental evidence shows that GR and sex hormone receptors share some common mechanisms of gene regulation, but they also exploit different mechanisms to repress pro-inflammatory genes depending on the target gene, cell type, and interactions with other TFs.

Estrogen receptor, AR, and GR induce expression of genes that control proliferation, differentiation, and cell death by directly binding to specific hormone response elements or by indirectly tethering through TFs, such as AP1, Sp1, Stat1, and NFκB. The potential crosstalk in the regulation of gene expression by GR and ER was studied mostly in non-immune cell types, which may, however, provide mechanistic evidence of the mechanisms potentially operating in cells of the immune system.

The functional interaction between GR and ER signaling has been observed in several cancer cell lines, and requires additional factors, such as MED14, SRC-2, and SRC-3 in the same complex, resulting in either cooperative or mutually inhibiting effects. GR may inhibit the action of ER via distinct mechanisms. GCs may inhibit the estrogen signaling indirectly, by inducing the estrogen-metabolizing enzyme in breast cancer cells. Synthetic GC dexamethasone (Dex) antagonizes ERα-regulated target gene expression in breast cancer cells treated with estrogen and Dex simultaneously via the direct protein–protein interaction and the recruitment of GR to ERα binding sites. This recruitment is facilitated by AP-1 and leads to a displacement of ERα from DNA and repression of its target genes transcription.

Reciprocally, the ER-mediated inhibition of the GR function was also described. Treatment of the breast cancer cell line with estrogen agonists downregulates GR protein levels via proteosome-mediated degradation. On the other hand, in an experimental lung inflammation rat model, the ER antagonist (ICI 182780) blocked the anti-inflammatory effects of GCs, suggesting that GR and ER co-operate in this setting in their anti-inflammatory activity. A subset of pro-inflammatory genes was repressed by both ER and GR (CD69, MCP-1, IL-6, IL-8), and the ER antagonist blocked Dex-mediated repression of these genes, by preventing the recruitment of nuclear coactivator 2 by the GR necessary for trans-repression. These data suggest that GR and ER functionally cooperate on selected promoters.

The functional effect of the interaction of GR with PR and ER is less characterized. PR and GR were shown to interact in vitro, and in vivo. Progesterone acts via GR to repress IL-1β-driven COX-2 activation. The AR and the GR form heterodimers at a common DNA site both in vitro and in vivo, and this interaction leads to mutual inhibition of transcriptional activity.

Conclusions

Most of the mechanistic insights into synergistic and antagonizing effects of GR and sex steroid receptors in gene expression were obtained in non-immune cells, and, to our knowledge, the interactions between GCs and sex hormones in immune cells have not been studied in vitro. However, receptors for both classes of hormones are present in variety of immune cells, where, as reviewed above, they have been separately shown to influence various aspect of immune cell activity, ranging from cell survival to differentiation and expression of pro- and anti-inflammatory molecules (Table 1). Thus, the investigation of possible mutual influence of GCs and sex hormones in immune cells and its mechanisms is warranted.

The effects of female sex hormones on cells of adaptive immune system such as Th cell differentiation and B cells may underlie the higher predisposition of women to AD. The GC-mediated suppression of Th1 and promotion of Treg cell activity, as well as apoptotic effects on B cells may explain in part the cellular basis of GCs’ efficacy in dampening the symptoms of many AD. Development of novel therapies for immune cell type- and gender-specific modulation of immune system may represent future direction for treatment of AD.

Author Contributions

OB, SB, and CR wrote and edited the manuscript.

Conflict of Interest Statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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  44. 44.

    Kovats S. Estrogen receptors regulate innate immune cells and signaling pathways. Cell Immunol (2015 ) 294(2):63–9.

    Not in our library10.1016/j.cellimm.2015.01.018

  45. 45.

    Cvoro A Tzagarakis-Foster C Tatomer D Paruthiyil S Fox MS Leitman DC. Distinct roles of unliganded and liganded estrogen receptors in transcriptional repression. Mol Cell (2006 ) 21(4):555–64.

    Not in our library10.1016/j.molcel.2006.01.014

  46. 46.

    Calippe B Douin-Echinard V Delpy L Laffargue M Lelu K Krust A 17Beta-estradiol promotes TLR4-triggered proinflammatory mediator production through direct estrogen receptor alpha signaling in macrophages in vivo. J Immunol (2010 ) 185(2):1169–76.

    Not in our library10.4049/jimmunol.0902383

  47. 47.

    Pratap UP Sharma HR Mohanty A Kale P Gopinath S Hima L Estrogen upregulates inflammatory signals through NF-kappaB, IFN-gamma, and nitric oxide via Akt/mTOR pathway in the lymph node lymphocytes of middle-aged female rats. Int Immunopharmacol (2015 ) 29(2):591–8.

    Not in our library10.1016/j.intimp.2015.09.024

  48. 48.

    Cvoro A Tatomer D Tee MK Zogovic T Harris HA Leitman DC. Selective estrogen receptor-beta agonists repress transcription of proinflammatory genes. J Immunol (2008 ) 180(1):630–6.

    Not in our library10.4049/jimmunol.180.1.630

  49. 49.

    Stein B Yang MX. Repression of the interleukin-6 promoter by estrogen receptor is mediated by NF-kappa B and C/EBP beta. Mol Cell Biol (1995 ) 15(9):4971–9.

    Not in our library10.1128/mcb.15.9.4971

  50. 50.

    An J Ribeiro RC Webb P Gustafsson JA Kushner PJ Baxter JD Estradiol repression of tumor necrosis factor-alpha transcription requires estrogen receptor activation function-2 and is enhanced by coactivators. Proc Natl Acad Sci U S A (1999 ) 96(26):15161–6.

    Not in our library10.1073/pnas.96.26.15161

  51. 51.

    Nettles KW Gil G Nowak J Metivier R Sharma VB Greene GL. CBP is a dosage-dependent regulator of nuclear factor-kappaB suppression by the estrogen receptor. Mol Endocrinol (2008 ) 22(2):263–72.

    Not in our library10.1210/me.2007-0324

  52. 52.

    Teilmann SC Clement CA Thorup J Byskov AG Christensen ST. Expression and localization of the progesterone receptor in mouse and human reproductive organs. J Endocrinol (2006 ) 191(3):525–35.

    Not in our library10.1677/joe.1.06565

  53. 53.

    Hardy DB Janowski BA Corey DR Mendelson CR. Progesterone receptor plays a major antiinflammatory role in human myometrial cells by antagonism of nuclear factor-kappaB activation of cyclooxygenase 2 expression. Mol Endocrinol (2006 ) 20(11):2724–33.

    Not in our library10.1210/me.2006-0112

  54. 54.

    Roubinian JR Talal N Greenspan JS Goodman JR Siiteri PK. Effect of castration and sex hormone treatment on survival, anti-nucleic acid antibodies, and glomerulonephritis in NZB/NZW F1 mice. J Exp Med (1978 ) 147(6):1568–83.

    Not in our library10.1084/jem.147.6.1568

  55. 55.

    Steinberg AD Roths JB Murphy ED Steinberg RT Raveche ES. Effects of thymectomy or androgen administration upon the autoimmune disease of MRL/Mp-lpr/lpr mice. J Immunol (1980 ) 125(2):871–3.

    Not in our library

  56. 56.

    Ariga H Edwards J Sullivan DA. Androgen control of autoimmune expression in lacrimal glands of MRL/Mp-lpr/lpr mice. Clin Immunol Immunopathol (1989 ) 53(3):499–508.

    Not in our library10.1016/0090-1229(89)90011-1

  57. 57.

    Fox HS. Androgen treatment prevents diabetes in nonobese diabetic mice. J Exp Med (1992 ) 175(5):1409–12.

    Not in our library10.1084/jem.175.5.1409

  58. 58.

    Chang CS Kokontis J Liao ST. Molecular cloning of human and rat complementary DNA encoding androgen receptors. Science (1988 ) 240(4850):324–6.

    Not in our library10.1126/science.3353726

  59. 59.

    MacLean HE Warne GL Zajac JD. Localization of functional domains in the androgen receptor. J Steroid Biochem Mol Biol (1997 ) 62(4):233–42.

    Not in our library10.1016/s0960-0760(97)00049-6

  60. 60.

    Liva SM Voskuhl RR. Testosterone acts directly on CD4+ T lymphocytes to increase IL-10 production. J Immunol (2001 ) 167(4):2060–7.

    Not in our library10.4049/jimmunol.167.4.2060

  61. 61.

    D’Agostino P Milano S Barbera C Di Bella G La Rosa M Ferlazzo V Sex hormones modulate inflammatory mediators produced by macrophages. Ann N Y Acad Sci (1999 ) 876:426–9.

    Not in our library10.1111/j.1749-6632.1999.tb07667.x

  62. 62.

    Lai JJ Lai KP Zeng W Chuang KH Altuwaijri S Chang C. Androgen receptor influences on body defense system via modulation of innate and adaptive immune systems: lessons from conditional AR knockout mice. Am J Pathol (2012 ) 181(5):1504–12.

    Not in our library10.1016/j.ajpath.2012.07.008

  63. 63.

    Straub RH Harle P Atzeni F Weidler C Cutolo M Sarzi-Puttini P Sex hormone concentrations in patients with rheumatoid arthritis are not normalized during 12 weeks of anti-tumor necrosis factor therapy. J Rheumatol (2005 ) 32(7):1253–8.

    Not in our library

  64. 64.

    Straub RH Vogl D Gross V Lang B Scholmerich J Andus T. Association of humoral markers of inflammation and dehydroepiandrosterone sulfate or cortisol serum levels in patients with chronic inflammatory bowel disease. Am J Gastroenterol (1998 ) 93(11):2197–202.

    Not in our library10.1111/j.1572-0241.1998.00535.x

  65. 65.

    Da Silva JA. Sex hormones and glucocorticoids: interactions with the immune system. Ann N Y Acad Sci (1999 ) 876:102–17; discussion 17–8.

    Not in our library10.1111/j.1749-6632.1999.tb07628.x

  66. 66.

    Barczyk K Ehrchen J Tenbrock K Ahlmann M Kneidl J Viemann D Glucocorticoids promote survival of anti-inflammatory macrophages via stimulation of adenosine receptor A3. Blood (2010 ) 116(3):446–55.

    Not in our library10.1182/blood-2009-10-247106

  67. 67.

    Zhou JY Zhong HJ Yang C Yan J Wang HY Jiang JX. Corticosterone exerts immunostimulatory effects on macrophages via endoplasmic reticulum stress. Br J Surg (2010 ) 97(2):281–93.

    Not in our library10.1002/bjs.6820

  68. 68.

    Migliorati G Nicoletti I D’Adamio F Spreca A Pagliacci C Riccardi C. Dexamethasone induces apoptosis in mouse natural killer cells and cytotoxic T lymphocytes. Immunology (1994 ) 81(1):21–6.

    Not in our library

  69. 69.

    Brokaw JJ White GW Baluk P Anderson GP Umemoto EY McDonald DM. Glucocorticoid-induced apoptosis of dendritic cells in the rat tracheal mucosa. Am J Respir Cell Mol Biol (1998 ) 19(4):598–605.

    Not in our library10.1165/ajrcmb.19.4.2870

  70. 70.

    Kim KD Choe YK Choe IS Lim JS. Inhibition of glucocorticoid-mediated, caspase-independent dendritic cell death by CD40 activation. J Leukoc Biol (2001 ) 69(3):426–34.

    Not in our library

  71. 71.

    Cao Y Bender IK Konstantinidis AK Shin SC Jewell CM Cidlowski JA Glucocorticoid receptor translational isoforms underlie maturational stage-specific glucocorticoid sensitivities of dendritic cells in mice and humans. Blood (2013 ) 121(9):1553–62.

    Not in our library10.1182/blood-2012-05-432336

  72. 72.

    Meagher LC Cousin JM Seckl JR Haslett C. Opposing effects of glucocorticoids on the rate of apoptosis in neutrophilic and eosinophilic granulocytes. J Immunol (1996 ) 156(11):4422–8.

    Not in our library

  73. 73.
    The Molecular Mechanisms of Glucocorticoids-Mediated Neutrophil Survival · 2011
    No notice
  74. 74.

    Jilma B Eichler HG Breiteneder H Wolzt M Aringer M Graninger W Effects of 17 beta-estradiol on circulating adhesion molecules. J Clin Endocrinol Metab (1994 ) 79(6):1619–24.

    Not in our library10.1210/jcem.79.6.7527406

  75. 75.

    Robinson DP Hall OJ Nilles TL Bream JH Klein SL 17beta-estradiol protects females against influenza by recruiting neutrophils and increasing virus-specific CD8 T cell responses in the lungs. J Virol (2014 ) 88(9):4711–20.

    Not in our library10.1128/jvi.02081-13

  76. 76.

    Baschant U Tuckermann J. The role of the glucocorticoid receptor in inflammation and immunity. J Steroid Biochem Mol Biol (2010 ) 120(2–3):69–75.

    Not in our library10.1016/j.jsbmb.2010.03.058

  77. 77.

    Perretti M Flower RJ. Measurement of lipocortin 1 levels in murine peripheral blood leukocytes by flow cytometry: modulation by glucocorticoids and inflammation. Br J Pharmacol (1996 ) 118(3):605–10.

    Not in our library10.1111/j.1476-5381.1996.tb15444.x

  78. 78.

    Shah S King EM Chandrasekhar A Newton R. Roles for the mitogen-activated protein kinase (MAPK) phosphatase, DUSP1, in feedback control of inflammatory gene expression and repression by dexamethasone. J Biol Chem (2014 ) 289(19):13667–79.

    Not in our library10.1074/jbc.m113.540799

  79. 79.

    Cho H Park OH Park J Ryu I Kim J Ko J Glucocorticoid receptor interacts with PNRC2 in a ligand-dependent manner to recruit UPF1 for rapid mRNA degradation. Proc Natl Acad Sci U S A (2015 ) 112(13):E1540–9.

    Not in our library10.1073/pnas.1409612112

  80. 80.

    Nakagawa M Bondy GP Waisman D Minshall D Hogg JC van Eeden SF. The effect of glucocorticoids on the expression of L-selectin on polymorphonuclear leukocyte. Blood (1999 ) 93(8):2730–7.

    Not in our library

  81. 81.

    Caramori G Adcock I. Anti-inflammatory mechanisms of glucocorticoids targeting granulocytes. Curr Drug Targets Inflamm Allergy (2005 ) 4(4):455–63.

    Not in our library10.2174/1568010054526331

  82. 82.

    Ricci E Ronchetti S Pericolini E Gabrielli E Cari L Gentili M Role of the glucocorticoid-induced leucine zipper gene in dexamethasone-induced inhibition of mouse neutrophil migration via control of annexin A1 expression. FASEB J (2017 ) 31(7):3054–65.

    Not in our library10.1096/fj.201601315r

  83. 83.

    Nadkarni S McArthur S. Oestrogen and immunomodulation: new mechanisms that impact on peripheral and central immunity. Curr Opin Pharmacol (2013 ) 13(4):576–81.

    Not in our library10.1016/j.coph.2013.05.007

  84. 84.

    MacNeil LG Baker SK Stevic I Tarnopolsky MA 17beta-estradiol attenuates exercise-induced neutrophil infiltration in men. Am J Physiol Regul Integr Comp Physiol (2011 ) 300(6):R1443–51.

    Not in our library10.1152/ajpregu.00689.2009

  85. 85.

    Chandrasekaran VR Periasamy S Liu LL Liu MY 17beta-Estradiol protects against acetaminophen-overdose-induced acute oxidative hepatic damage and increases the survival rate in mice. Steroids (2011 ) 76(1–2):118–24.

    Not in our library10.1016/j.steroids.2010.09.008

  86. 86.

    Sheh A Ge Z Parry NM Muthupalani S Rager JE Raczynski AR 17beta-Estradiol and tamoxifen prevent gastric cancer by modulating leukocyte recruitment and oncogenic pathways in Helicobacter pylori-infected INS-GAS male mice. Cancer Prev Res (Phila) (2011 ) 4(9):1426–35.

    Not in our library10.1158/1940-6207.capr-11-0219

  87. 87.

    Shih HC Huang MS Lee CH. Estrogen augments the protection of hypertonic saline treatment from mesenteric ischemia-reperfusion injury. Shock (2011 ) 35(3):302–7.

    Not in our library10.1097/shk.0b013e3181f8b420

  88. 88.

    Yang SJ Chen HM Hsieh CH Hsu JT Yeh CN Yeh TS Akt pathway is required for oestrogen-mediated attenuation of lung injury in a rodent model of cerulein-induced acute pancreatitis. Injury (2011 ) 42(7):638–42.

    Not in our library10.1016/j.injury.2010.07.242

  89. 89.

    Pioli PA Jensen AL Weaver LK Amiel E Shen Z Shen L Estradiol attenuates lipopolysaccharide-induced CXC chemokine ligand 8 production by human peripheral blood monocytes. J Immunol (2007 ) 179(9):6284–90.

    Not in our library10.4049/jimmunol.179.9.6284

  90. 90.

    Doucet D Badami C Palange D Bonitz RP Lu Q Xu DZ Estrogen receptor hormone agonists limit trauma hemorrhage shock-induced gut and lung injury in rats. PLoS One (2010 ) 5(2):e9421.

    Not in our library10.1371/journal.pone.0009421

  91. 91.

    Xing D Gong K Feng W Nozell SE Chen YF Chatham JC O-GlcNAc modification of NFkappaB p65 inhibits TNF-alpha-induced inflammatory mediator expression in rat aortic smooth muscle cells. PLoS One (2011 ) 6(8):e24021

    Not in our library10.1371/journal.pone.0024021

  92. 92.

    Golecka-Bakowska M Mierzwinska-Nastalska E Bychawska M Influence of hormone supplementation therapy on the incidence of denture stomatitis and on chemiluminescent activity of polymorphonuclear granulocytes in blood of menopausal-aged women. Eur J Med Res (2010 ) 15(Suppl 2):46–9.

    Not in our library10.1186/2047-783x-15-s2-46

  93. 93.

    Nadkarni S Cooper D Brancaleone V Bena S Perretti M. Activation of the annexin A1 pathway underlies the protective effects exerted by estrogen in polymorphonuclear leukocytes. Arterioscler Thromb Vasc Biol (2011 ) 31(11):2749–59.

    Not in our library10.1161/atvbaha.111.235176

  94. 94.

    Rogers A Eastell R. The effect of 17beta-estradiol on production of cytokines in cultures of peripheral blood. Bone (2001 ) 29(1):30–4.

    Not in our library10.1016/s8756-3282(01)00468-9

  95. 95.

    Asai K Hiki N Mimura Y Ogawa T Unou K Kaminishi M. Gender differences in cytokine secretion by human peripheral blood mononuclear cells: role of estrogen in modulating LPS-induced cytokine secretion in an ex vivo septic model. Shock (2001 ) 16(5):340–3.

    Not in our library10.1097/00024382-200116050-00003

  96. 96.

    Toyoda Y Miyashita T Endo S Tsuneyama K Fukami T Nakajima M Estradiol and progesterone modulate halothane-induced liver injury in mice. Toxicol Lett (2011 ) 204(1):17–24.

    Not in our library10.1016/j.toxlet.2011.03.031

  97. 97.

    Murphy AJ Guyre PM Pioli PA. Estradiol suppresses NF-kappa B activation through coordinated regulation of let-7a and miR-125b in primary human macrophages. J Immunol (2010 ) 184(9):5029–37.

    Not in our library10.4049/jimmunol.0903463

  98. 98.

    Hsu JT Kan WH Hsieh CH Choudhry MA Schwacha MG Bland KI Mechanism of estrogen-mediated attenuation of hepatic injury following trauma-hemorrhage: Akt-dependent HO-1 up-regulation. J Leukoc Biol (2007 ) 82(4):1019–26.

    Not in our library10.1189/jlb.0607355

  99. 99.

    Cuzzocrea S Genovese T Mazzon E Esposito E Di Paola R Muia C Effect of 17beta-estradiol on signal transduction pathways and secondary damage in experimental spinal cord trauma. Shock (2008 ) 29(3):362–71.

    Not in our library10.1097/shk.0b013e31814545dc

  100. 100.

    Woltman AM de Fijter JW Kamerling SW Paul LC Daha MR van Kooten C. The effect of calcineurin inhibitors and corticosteroids on the differentiation of human dendritic cells. Eur J Immunol (2000 ) 30(7):1807–12.

    Not in our library10.1002/1521-4141(200007)30:7<1807::aid-immu1807>3.0.co;2-n

  101. 101.

    Chen L Hasni MS Jondal M Yakimchuk K. Modification of anti-tumor immunity by tolerogenic dendritic cells. Autoimmunity (2017 ) 50(6):370–6.

    Not in our library10.1080/08916934.2017.1344837

  102. 102.

    Bros M Jahrling F Renzing A Wiechmann N Dang NA Sutter A A newly established murine immature dendritic cell line can be differentiated into a mature state, but exerts tolerogenic function upon maturation in the presence of glucocorticoid. Blood (2007 ) 109(9):3820–9.

    Not in our library10.1182/blood-2006-07-035576

  103. 103.

    Vanderheyde N Verhasselt V Goldman M Willems F. Inhibition of human dendritic cell functions by methylprednisolone. Transplantation (1999 ) 67(10):1342–7.

    Not in our library10.1097/00007890-199905270-00009

  104. 104.

    Seillet C Rouquie N Foulon E Douin-Echinard V Krust A Chambon P Estradiol promotes functional responses in inflammatory and steady-state dendritic cells through differential requirement for activation function-1 of estrogen receptor alpha. J Immunol (2013 ) 190(11):5459–70.

    Not in our library10.4049/jimmunol.1203312

  105. 105.

    Siracusa MC Overstreet MG Housseau F Scott AL Klein SL. 17beta-estradiol alters the activity of conventional and IFN-producing killer dendritic cells. J Immunol (2008 ) 180(3):1423–31.

    Not in our library10.4049/jimmunol.180.3.1423

  106. 106.

    Cunningham MA Naga OS Eudaly JG Scott JL Gilkeson GS. Estrogen receptor alpha modulates toll-like receptor signaling in murine lupus. Clin Immunol (2012 ) 144(1):1–12.

    Not in our library10.1016/j.clim.2012.04.001

  107. 107.

    Douin-Echinard V Laffont S Seillet C Delpy L Krust A Chambon P Estrogen receptor alpha, but not beta, is required for optimal dendritic cell differentiation and [corrected] CD40-induced cytokine production. J Immunol (2008 ) 180(6):3661–9.

    Not in our library10.4049/jimmunol.180.6.3661

  108. 108.

    Delpy L Douin-Echinard V Garidou L Bruand C Saoudi A Guery JC. Estrogen enhances susceptibility to experimental autoimmune myasthenia gravis by promoting type 1-polarized immune responses. J Immunol (2005 ) 175(8):5050–7.

    Not in our library10.4049/jimmunol.175.8.5050

  109. 109.

    Liu HY Buenafe AC Matejuk A Ito A Zamora A Dwyer J Estrogen inhibition of EAE involves effects on dendritic cell function. J Neurosci Res (2002 ) 70(2):238–48.

    Not in our library10.1002/jnr.10409

  110. 110.

    Bachy V Williams DJ Ibrahim MA. Altered dendritic cell function in normal pregnancy. J Reprod Immunol (2008 ) 78(1):11–21.

    Not in our library10.1016/j.jri.2007.09.004

  111. 111.

    Papenfuss TL Powell ND McClain MA Bedarf A Singh A Gienapp IE Estriol generates tolerogenic dendritic cells in vivo that protect against autoimmunity. J Immunol (2011 ) 186(6):3346–55.

    Not in our library10.4049/jimmunol.1001322

  112. 112.

    Subramanian S Yates M Vandenbark AA Offner H. Oestrogen-mediated protection of experimental autoimmune encephalomyelitis in the absence of Foxp3+ regulatory T cells implicates compensatory pathways including regulatory B cells. Immunology (2011 ) 132(3):340–7.

    Not in our library10.1111/j.1365-2567.2010.03380.x

  113. 113.

    Brewer JA Kanagawa O Sleckman BP Muglia LJ. Thymocyte apoptosis induced by T cell activation is mediated by glucocorticoids in vivo. J Immunol (2002 ) 169(4):1837–43.

    Not in our library10.4049/jimmunol.169.4.1837

  114. 114.

    Vacchio MS Ashwell JD Glucocorticoids and thymocyte development. Semin Immunol (2000 ) 12(5):475–85.

    Not in our library10.1006/smim.2000.0265

  115. 115.

    Caron-Leslie LM Schwartzman RA Gaido ML Compton MM Cidlowski JA. Identification and characterization of glucocorticoid-regulated nuclease(s) in lymphoid cells undergoing apoptosis. J Steroid Biochem Mol Biol (1991 ) 40(4–6):661–71.

    Not in our library10.1016/0960-0760(91)90288-g

  116. 116.

    Brunetti M Martelli N Colasante A Piantelli M Musiani P Aiello FB. Spontaneous and glucocorticoid-induced apoptosis in human mature T lymphocytes. Blood (1995 ) 86(11):4199–205.

    Not in our library

  117. 117.

    Stephens GL Ignatowicz L. Decreasing the threshold for thymocyte activation biases CD4+ T cells toward a regulatory (CD4+CD25+) lineage. Eur J Immunol (2003 ) 33(5):1282–91.

    Not in our library10.1002/eji.200323927

  118. 118.

    Cohen JJ Duke RC. Glucocorticoid activation of a calcium-dependent endonuclease in thymocyte nuclei leads to cell death. J Immunol (1984 ) 132(1):38–42.

    Not in our library

  119. 119.

    Wyllie AH. Glucocorticoid-induced thymocyte apoptosis is associated with endogenous endonuclease activation. Nature (1980 ) 284(5756):555–6.

    Not in our library10.1038/284555a0

  120. 120.

    Ashwell JD Lu FW Vacchio MS. Glucocorticoids in T cell development and function*. Annu Rev Immunol (2000 ) 18:309–45.

    Not in our library10.1146/annurev.immunol.18.1.309

  121. 121.

    Van Laethem F Baus E Smyth LA Andris F Bex F Urbain J Glucocorticoids attenuate T cell receptor signaling. J Exp Med (2001 ) 193(7):803–14.

    Not in our library10.1084/jem.193.7.803

  122. 122.

    Chen Y Qiao S Tuckermann J Okret S Jondal M. Thymus-derived glucocorticoids mediate androgen effects on thymocyte homeostasis. FASEB J (2010 ) 24(12):5043–51.

    Not in our library10.1096/fj.10-168724

  123. 123.

    Aboussaouira T Marie C Brugal G Idelman S. Inhibitory effect of 17 beta-estradiol on thymocyte proliferation and metabolic activity in young rats. Thymus (1991 ) 17(3):167–80.

    Not in our library

  124. 124.

    Okuyama R Abo T Seki S Ohteki T Sugiura K Kusumi A Estrogen administration activates extrathymic T cell differentiation in the liver. J Exp Med (1992 ) 175(3):661–9.

    Not in our library10.1084/jem.175.3.661

  125. 125.

    Phuc LH Papiernik M Berrih S Duval D. Thymic involution in pregnant mice. I. Characterization of the remaining thymocyte subpopulations. Clin Exp Immunol (1981 ) 44(2):247–52.

    Not in our library

  126. 126.

    Phuc LH Papiernik M Dardenne M. Thymic involution in pregnant mice. II. Functional aspects of the remaining thymocytes. Clin Exp Immunol (1981 ) 44(2):253–61.

    Not in our library

  127. 127.

    Olsen NJ Viselli SM Shults K Stelzer G Kovacs WJ. Induction of immature thymocyte proliferation after castration of normal male mice. Endocrinology (1994 ) 134(1):107–13.

    Not in our library10.1210/endo.134.1.8275924

  128. 128.

    Britanova OV Shugay M Merzlyak EM Staroverov DB Putintseva EV Turchaninova MA Dynamics of individual T cell repertoires: from cord blood to centenarians. J Immunol (2016 ) 196(12):5005–13.

    Not in our library10.4049/jimmunol.1600005

  129. 129.

    Zhu J Yamane H Paul WE. Differentiation of effector CD4 T cell populations (*). Annu Rev Immunol (2010 ) 28:445–89.

    Not in our library10.1146/annurev-immunol-030409-101212

  130. 130.

    Elenkov IJ. Glucocorticoids and the Th1/Th2 balance. Ann N Y Acad Sci (2004 ) 1024:138–46.

    Not in our library10.1196/annals.1321.010

  131. 131.

    Refojo D Liberman AC Giacomini D Carbia Nagashima A Graciarena M Echenique C Integrating systemic information at the molecular level: cross-talk between steroid receptors and cytokine signaling on different target cells. Ann N Y Acad Sci (2003 ) 992:196–204.

    Not in our library10.1111/j.1749-6632.2003.tb03150.x

  132. 132.

    Almawi WY Melemedjian OK Rieder MJ. An alternate mechanism of glucocorticoid anti-proliferative effect: promotion of a Th2 cytokine-secreting profile. Clin Transplant (1999 ) 13(5):365–74.

    Not in our library10.1034/j.1399-0012.1999.130501.x

  133. 133.

    Liberman AC Refojo D Druker J Toscano M Rein T Holsboer F The activated glucocorticoid receptor inhibits the transcription factor T-bet by direct protein-protein interaction. FASEB J (2007 ) 21(4):1177–88.

    Not in our library10.1096/fj.06-7452com

  134. 134.

    Liu M Hu X Wang Y Peng F Yang Y Chen X Effect of high-dose methylprednisolone treatment on Th17 cells in patients with multiple sclerosis in relapse. Acta Neurol Scand (2009 ) 120(4):235–41.

    Not in our library10.1111/j.1600-0404.2009.01158.x

  135. 135.

    Banuelos J Cao Y Shin SC Lu NZ. Immunopathology alters Th17 cell glucocorticoid sensitivity. Allergy (2017 ) 72(3):331–41.

    Not in our library10.1111/all.13051

  136. 136.

    Bereshchenko O Coppo M Bruscoli S Biagioli M Cimino M Frammartino T GILZ promotes production of peripherally induced Treg cells and mediates the crosstalk between glucocorticoids and TGF-beta signaling. Cell Rep (2014 ) 7(2):464–75.

    Not in our library10.1016/j.celrep.2014.03.004

  137. 137.

    Ugor E Prenek L Pap R Berta G Ernszt D Najbauer J Glucocorticoid hormone treatment enhances the cytokine production of regulatory T cells by upregulation of Foxp3 expression. Immunobiology (2018 ) 223(4–5):422–31.

    Not in our library10.1016/j.imbio.2017.10.010

  138. 138.

    Chen X Oppenheim JJ Winkler-Pickett RT Ortaldo JR Howard OM. Glucocorticoid amplifies IL-2-dependent expansion of functional FoxP3(+)CD4(+)CD25(+) T regulatory cells in vivo and enhances their capacity to suppress EAE. Eur J Immunol (2006 ) 36(8):2139–49.

    Not in our library10.1002/eji.200635873

  139. 139.

    Chung IY Dong HF Zhang X Hassanein NM Howard OM Oppenheim JJ Effects of IL-7 and dexamethasone: induction of CD25, the high affinity IL-2 receptor, on human CD4+ cells. Cell Immunol (2004 ) 232(1–2):57–63.

    Not in our library10.1016/j.cellimm.2005.01.011

  140. 140.

    Stary G Klein I Bauer W Koszik F Reininger B Kohlhofer S Glucocorticosteroids modify Langerhans cells to produce TGF-beta and expand regulatory T cells. J Immunol (2011 ) 186(1):103–12.

    Not in our library10.4049/jimmunol.1002485

  141. 141.

    Suarez A Lopez P Gomez J Gutierrez C. Enrichment of CD4+ CD25high T cell population in patients with systemic lupus erythematosus treated with glucocorticoids. Ann Rheum Dis (2006 ) 65(11):1512–7.

    Not in our library10.1136/ard.2005.049924

  142. 142.

    de Paz B Alperi-Lopez M Ballina-Garcia FJ Prado C Gutierrez C Suarez A. Cytokines and regulatory T cells in rheumatoid arthritis and their relationship with response to corticosteroids. J Rheumatol (2010 ) 37(12):2502–10.

    Not in our library10.3899/jrheum.100324

  143. 143.

    Hu Y Tian W Zhang LL Liu H Yin GP He BS Function of regulatory T-cells improved by dexamethasone in Graves’ disease. Eur J Endocrinol (2012 ) 166(4):641–6.

    Not in our library10.1530/eje-11-0879

  144. 144.

    Cannarile L Cuzzocrea S Santucci L Agostini M Mazzon E Esposito E Glucocorticoid-induced leucine zipper is protective in Th1-mediated models of colitis. Gastroenterology (2009 ) 136(2):530–41.

    Not in our library10.1053/j.gastro.2008.09.024

  145. 145.

    Cannarile L Fallarino F Agostini M Cuzzocrea S Mazzon E Vacca C Increased GILZ expression in transgenic mice up-regulates Th-2 lymphokines. Blood (2006 ) 107(3):1039–47.

    Not in our library10.1182/blood-2005-05-2183

  146. 146.

    Lelu K Laffont S Delpy L Paulet PE Perinat T Tschanz SA Estrogen receptor alpha signaling in T lymphocytes is required for estradiol-mediated inhibition of Th1 and Th17 cell differentiation and protection against experimental autoimmune encephalomyelitis. J Immunol (2011 ) 187(5):2386–93.

    Not in our library10.4049/jimmunol.1101578

  147. 147.

    Priyanka HP Krishnan HC Singh RV Hima L Thyagarajan S. Estrogen modulates in vitro T cell responses in a concentration- and receptor-dependent manner: effects on intracellular molecular targets and antioxidant enzymes. Mol Immunol (2013 ) 56(4):328–39.

    Not in our library10.1016/j.molimm.2013.05.226

  148. 148.

    Karpuzoglu-Sahin E Zhi-Jun Y Lengi A Sriranganathan N Ansar Ahmed S. Effects of long-term estrogen treatment on IFN-gamma, IL-2 and IL-4 gene expression and protein synthesis in spleen and thymus of normal C57BL/6 mice. Cytokine (2001 ) 14(4):208–17.

    Not in our library10.1006/cyto.2001.0876

  149. 149.

    Grasso G Muscettola M The influence of beta-estradiol and progesterone on interferon gamma production in vitro. Int J Neurosci (1990 ) 51(3–4):315–7.

    Not in our library10.3109/00207459008999730

  150. 150.

    Fox HS Bond BL Parslow TG. Estrogen regulates the IFN-gamma promoter. J Immunol (1991 ) 146(12):4362–7.

    Not in our library

  151. 151.

    Karpuzoglu-Sahin E Hissong BD Ansar Ahmed S. Interferon-gamma levels are upregulated by 17-beta-estradiol and diethylstilbestrol. J Reprod Immunol (2001 ) 52(1–2):113–27.

    Not in our library10.1016/s0165-0378(01)00117-6

  152. 152.

    Maret A Coudert JD Garidou L Foucras G Gourdy P Krust A Estradiol enhances primary antigen-specific CD4 T cell responses and Th1 development in vivo. Essential role of estrogen receptor alpha expression in hematopoietic cells. Eur J Immunol (2003 ) 33(2):512–21.

    Not in our library10.1002/immu.200310027

  153. 153.

    Karpuzoglu E Phillips RA Gogal RM Jr Ansar Ahmed S. IFN-gamma-inducing transcription factor, T-bet is upregulated by estrogen in murine splenocytes: role of IL-27 but not IL-12. Mol Immunol (2007 ) 44(7):1808–14.

    Not in our library10.1016/j.molimm.2006.08.005

  154. 154.

    Dai R Phillips RA Zhang Y Khan D Crasta O Ahmed SA. Suppression of LPS-induced interferon-gamma and nitric oxide in splenic lymphocytes by select estrogen-regulated microRNAs: a novel mechanism of immune modulation. Blood (2008 ) 112(12):4591–7.

    Not in our library10.1182/blood-2008-04-152488

  155. 155.

    Marzi M Vigano A Trabattoni D Villa ML Salvaggio A Clerici E Characterization of type 1 and type 2 cytokine production profile in physiologic and pathologic human pregnancy. Clin Exp Immunol (1996 ) 106(1):127–33.

    Not in our library10.1046/j.1365-2249.1996.d01-809.x

  156. 156.

    Matalka KZ. The effect of estradiol, but not progesterone, on the production of cytokines in stimulated whole blood, is concentration-dependent. Neuro Endocrinol Lett (2003 ) 24(3–4):185–91.

    Not in our library

  157. 157.

    Sabahi F Rola-Plesczcynski M O’Connell S Frenkel LD. Qualitative and quantitative analysis of T lymphocytes during normal human pregnancy. Am J Reprod Immunol (1995 ) 33(5):381–93.

    Not in our library10.1111/j.1600-0897.1995.tb00907.x

  158. 158.

    Lou Y Hu M Wang Q Yuan M Wang N Le F Estradiol suppresses TLR4-triggered apoptosis of decidual stromal cells and drives an anti-inflammatory TH2 shift by activating SGK1. Int J Biol Sci (2017 ) 13(4):434–48.

    Not in our library10.7150/ijbs.18278

  159. 159.

    Konermann A Winter J Novak N Allam JP Jager A. Verification of IL-17A and IL-17F in oral tissues and modulation of their expression pattern by steroid hormones. Cell Immunol (2013 ) 285(1–2):133–40.

    Not in our library10.1016/j.cellimm.2013.10.004

  160. 160.

    Wang Y Cela E Gagnon S Sweezey NB. Estrogen aggravates inflammation in Pseudomonas aeruginosa pneumonia in cystic fibrosis mice. Respir Res (2010 ) 11:166.

    Not in our library10.1186/1465-9921-11-166

  161. 161.

    Molnar I Bohaty I Somogyine-Vari E. High prevalence of increased interleukin-17A serum levels in postmenopausal estrogen deficiency. Menopause (2014 ) 21(7):749–52.

    Not in our library10.1097/gme.0000000000000125

  162. 162.

    Polanczyk MJ Hopke C Huan J Vandenbark AA Offner H. Enhanced FoxP3 expression and Treg cell function in pregnant and estrogen-treated mice. J Neuroimmunol (2005 ) 170(1–2):85–92.

    Not in our library10.1016/j.jneuroim.2005.08.023

  163. 163.

    Tai P Wang J Jin H Song X Yan J Kang Y Induction of regulatory T cells by physiological level estrogen. J Cell Physiol (2008 ) 214(2):456–64.

    Not in our library10.1002/jcp.21221

  164. 164.

    Adurthi S Kumar MM Vinodkumar HS Mukherjee G Krishnamurthy H Acharya KK Oestrogen receptor-alpha binds the FOXP3 promoter and modulates regulatory T-cell function in human cervical cancer. Sci Rep (2017 ) 7(1):17289

    Not in our library10.1038/s41598-017-17102-w

  165. 165.

    Polanczyk MJ Carson BD Subramanian S Afentoulis M Vandenbark AA Ziegler SF Cutting edge: estrogen drives expansion of the CD4+CD25+ regulatory T cell compartment. J Immunol (2004 ) 173(4):2227–30.

    Not in our library10.4049/jimmunol.173.4.2227

  166. 166.

    Polanczyk MJ Hopke C Vandenbark AA Offner H. Treg suppressive activity involves estrogen-dependent expression of programmed death-1 (PD-1). Int Immunol (2007 ) 19(3):337–43.

    Not in our library10.1093/intimm/dxl151

  167. 167.

    Gruver-Yates AL Quinn MA Cidlowski JA. Analysis of glucocorticoid receptors and their apoptotic response to dexamethasone in male murine B cells during development. Endocrinology (2014 ) 155(2):463–74.

    Not in our library10.1210/en.2013-1473

  168. 168.

    Lill-Elghanian D Schwartz K King L Fraker P. Glucocorticoid-induced apoptosis in early B cells from human bone marrow. Exp Biol Med (Maywood) (2002 ) 227(9):763–70.

    Not in our library10.1177/153537020222700907

  169. 169.

    Smith LK Cidlowski JA. Glucocorticoid-induced apoptosis of healthy and malignant lymphocytes. Prog Brain Res (2010 ) 182:1–30.

    Not in our library10.1016/s0079-6123(10)82001-1

  170. 170.

    Bruscoli S Biagioli M Sorcini D Frammartino T Cimino M Sportoletti P Lack of glucocorticoid-induced leucine zipper (GILZ) deregulates B-cell survival and results in B-cell lymphocytosis in mice. Blood (2015 ) 126(15):1790–801.

    Not in our library10.1182/blood-2015-03-631580

  171. 171.

    Barnes PJ Corticosteroids, IgE, and atopy. J Clin Invest (2001 ) 107(3):265–6.

    Not in our library10.1172/jci12157

  172. 172.

    Jabara HH Brodeur SR Geha RS. Glucocorticoids upregulate CD40 ligand expression and induce CD40L-dependent immunoglobulin isotype switching. J Clin Invest (2001 ) 107(3):371–8.

    Not in our library10.1172/jci10168

  173. 173.

    Charmandari E Tsigos C Chrousos G. Endocrinology of the stress response. Annu Rev Physiol (2005 ) 67:259–84.

    Not in our library10.1146/annurev.physiol.67.040403.120816

  174. 174.
    Estrogen up-regulates Bcl-2 and blocks tolerance induction of naïve B cells · 2000
    Not checked
  175. 175.

    Grimaldi CM Michael DJ Diamond B. Cutting edge: expansion and activation of a population of autoreactive marginal zone B cells in a model of estrogen-induced lupus. J Immunol (2001 ) 167(4):1886–90.

    Not in our library10.4049/jimmunol.167.4.1886

  176. 176.

    Grimaldi CM Cleary J Dagtas AS Moussai D Diamond B. Estrogen alters thresholds for B cell apoptosis and activation. J Clin Invest (2002 ) 109(12):1625–33.

    Not in our library10.1172/jci0214873

  177. 177.

    Grimaldi CM Jeganathan V Diamond B. Hormonal regulation of B cell development: 17 beta-estradiol impairs negative selection of high-affinity DNA-reactive B cells at more than one developmental checkpoint. J Immunol (2006 ) 176(5):2703–10.

    Not in our library10.4049/jimmunol.176.5.2703

  178. 178.

    Klose CS Artis D. Innate lymphoid cells as regulators of immunity, inflammation and tissue homeostasis. Nat Immunol (2016 ) 17(7):765–74.

    Not in our library10.1038/ni.3489

  179. 179.

    Bartemes K Chen CC Iijima K Drake L Kita H. IL-33-responsive group 2 innate lymphoid cells are regulated by female sex hormones in the uterus. J Immunol (2018 ) 200(1):229–36.

    Not in our library10.4049/jimmunol.1602085

  180. 180.

    Li BW Hendriks RW. Group 2 innate lymphoid cells in lung inflammation. Immunology (2013 ) 140(3):281–7.

    Not in our library10.1111/imm.12153

  181. 181.

    Laffont S Blanquart E Savignac M Cenac C Laverny G Metzger D Androgen signaling negatively controls group 2 innate lymphoid cells. J Exp Med (2017 ) 214(6):1581–92.

    Not in our library10.1084/jem.20161807

  182. 182.

    Evans RM. The steroid and thyroid hormone receptor superfamily. Science (1988 ) 240(4854):889–95.

    Not in our library10.1126/science.3283939

  183. 183.

    Nilsson S Makela S Treuter E Tujague M Thomsen J Andersson G Mechanisms of estrogen action. Physiol Rev (2001 ) 81(4):1535–65.

    Not in our library10.1152/physrev.2001.81.4.1535

  184. 184.

    Kushner PJ Agard DA Greene GL Scanlan TS Shiau AK Uht RM Estrogen receptor pathways to AP-1. J Steroid Biochem Mol Biol (2000 ) 74(5):311–7.

    Not in our library10.1016/s0960-0760(00)00108-4

  185. 185.

    Kerppola TK Luk D Curran T. Fos is a preferential target of glucocorticoid receptor inhibition of AP-1 activity in vitro. Mol Cell Biol (1993 ) 13(6):3782–91.

    Not in our library10.1128/mcb.13.6.3782

  186. 186.

    Safe S. Transcriptional activation of genes by 17 beta-estradiol through estrogen receptor-Sp1 interactions. Vitam Horm (2001 ) 62:231–52.

    Not in our library10.1016/s0083-6729(01)62006-5

  187. 187.

    Ou XM Chen K Shih JC. Glucocorticoid and androgen activation of monoamine oxidase A is regulated differently by R1 and Sp1. J Biol Chem (2006 ) 281(30):21512–25.

    Not in our library10.1074/jbc.m600250200

  188. 188.

    Wyszomierski SL Yeh J Rosen JM. Glucocorticoid receptor/signal transducer and activator of transcription 5 (STAT5) interactions enhance STAT5 activation by prolonging STAT5 DNA binding and tyrosine phosphorylation. Mol Endocrinol (1999 ) 13(2):330–43.

    Not in our library10.1210/mend.13.2.0232

  189. 189.

    Biswas DK Singh S Shi Q Pardee AB Iglehart JD. Crossroads of estrogen receptor and NF-kappaB signaling. Sci STKE (2005 ) 2005(288):pe27.

    Not in our library10.1126/stke.2882005pe27

  190. 190.

    McKay LI Cidlowski JA. Cross-talk between nuclear factor-kappa B and the steroid hormone receptors: mechanisms of mutual antagonism. Mol Endocrinol (1998 ) 12(1):45–56.

    Not in our library10.1210/me.12.1.45

  191. 191.

    Bolt MJ Stossi F Newberg JY Orjalo A Johansson HE Mancini MA. Coactivators enable glucocorticoid receptor recruitment to fine-tune estrogen receptor transcriptional responses. Nucleic Acids Res (2013 ) 41(7):4036–48.

    Not in our library10.1093/nar/gkt100

  192. 192.

    Gong H Jarzynka MJ Cole TJ Lee JH Wada T Zhang B Glucocorticoids antagonize estrogens by glucocorticoid receptor-mediated activation of estrogen sulfotransferase. Cancer Res (2008 ) 68(18):7386–93.

    Not in our library10.1158/0008-5472.can-08-1545

  193. 193.
    Interaction of Glucocorticoid Receptor (GR) with Estrogen Receptor (ER) α and Activator Protein 1 (AP1) in Dexamethasone-mediated Interference of ERα Activity · 2013
    No notice
  194. 194.

    Uht RM Anderson CM Webb P Kushner PJ. Transcriptional activities of estrogen and glucocorticoid receptors are functionally integrated at the AP-1 response element. Endocrinology (1997 ) 138(7):2900–8.

    Not in our library10.1210/endo.138.7.5244

  195. 195.

    Kinyamu HK Archer TK. Estrogen receptor-dependent proteasomal degradation of the glucocorticoid receptor is coupled to an increase in mdm2 protein expression. Mol Cell Biol (2003 ) 23(16):5867–81.

    Not in our library10.1128/mcb.23.16.5867-5881.2003

  196. 196.

    Cuzzocrea S Bruscoli S Crisafulli C Mazzon E Agostini M Muia C Estrogen receptor antagonist fulvestrant (ICI 182,780) inhibits the anti-inflammatory effect of glucocorticoids. Mol Pharmacol (2007 ) 71(1):132–44.

    Not in our library10.1124/mol.106.029629

  197. 197.

    Cvoro A Yuan C Paruthiyil S Miller OH Yamamoto KR Leitman DC. Cross talk between glucocorticoid and estrogen receptors occurs at a subset of proinflammatory genes. J Immunol (2011 ) 186(7):4354–60.

    Not in our library10.4049/jimmunol.1002205

  198. 198.

    Lei K Chen L Georgiou EX Sooranna SR Khanjani S Brosens JJ Progesterone acts via the nuclear glucocorticoid receptor to suppress IL-1beta-induced COX-2 expression in human term myometrial cells. PLoS One (2012 ) 7(11):e50167

    Not in our library10.1371/journal.pone.0050167

  199. 199.

    Demirpence E Semlali A Oliva J Balaguer P Badia E Duchesne MJ An estrogen-responsive element-targeted histone deacetylase enzyme has an antiestrogen activity that differs from that of hydroxytamoxifen. Cancer Res (2002 ) 62(22):6519–28.

    Not in our library

  200. 200.

    Chen S Wang J Yu G Liu W Pearce D. Androgen and glucocorticoid receptor heterodimer formation. A possible mechanism for mutual inhibition of transcriptional activity. J Biol Chem (1997 ) 272(22):14087–92.

    Not in our library10.1074/jbc.272.22.14087

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