ArticleImmunology2011
Oestrogen-mediated protection of experimental autoimmune encephalomyelitis in the absence of Foxp3+ regulatory T cells implicates compensatory pathways including regulatory B cells.
Article in Immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- The Immunomodulatory Role of Estrogen in Malaria: A Review of Sex Differences and Therapeutic Implications.Immunity, inflammation and disease · 2025Review
- Sex as a biological variable: Mechanistic insights and clinical relevance in solid organ transplantation.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2023Review
- Sex differences in a murine model of asthma are time and tissue compartment dependent.PloS one · 2023Article
- Sex bias in lymphocytes: Implications for autoimmune diseases.Frontiers in immunology · 2022Review
- Sex, Cells, and Asthma.Mayo Clinic proceedings · 2021Review
- CCR6 blockade on regulatory T cells ameliorates experimental model of multiple sclerosis.Central-European journal of immunology · 2020Article
- Estrogen-induced compensatory mechanisms protect IL-10-deficient mice from developing EAE.Journal of neuroinflammation · 2019Article
- Sex bias in autoimmunity.Current opinion in rheumatology · 2019Review
- Immunological Processes Driving IgE Sensitisation and Disease Development in Males and Females.International journal of molecular sciences · 2018Review
- Glucocorticoids, Sex Hormones, and Immunity.Frontiers in immunology · 2018Review
- Estrogen protects both sexes against EAE by promoting common regulatory cell subtypes independent of endogenous estrogen.Metabolic brain disease · 2017Article
- Estrogen protection against EAE modulates the microbiota and mucosal-associated regulatory cells.Journal of neuroimmunology · 2017Article
- Sex differences in stroke across the lifespan: The role of T lymphocytes.Neurochemistry international · 2017Review
- Novel feedback loop between M2 macrophages/microglia and regulatory B cells in estrogen-protected EAE mice.Journal of neuroimmunology · 2017Article
- Regulatory B Cells in Pregnancy: Lessons from Autoimmunity, Graft Tolerance, and Cancer.Frontiers in immunology · 2017Review
- Estrogen induces multiple regulatory B cell subtypes and promotes M2 microglia and neuroprotection during experimental autoimmune encephalomyelitis.Journal of neuroimmunology · 2016Article
- Treatment with IL-10 producing B cells in combination with E2 ameliorates EAE severity and decreases CNS inflammation in B cell-deficient mice.Metabolic brain disease · 2015Article
- Regulatory CD8(+)CD122 (+) T-cells predominate in CNS after treatment of experimental stroke in male mice with IL-10-secreting B-cells.Metabolic brain disease · 2015Article
- Epigenetic Regulation of Non-Lymphoid Cells by Bisphenol A, a Model Endocrine Disrupter: Potential Implications for Immunoregulation.Frontiers in endocrinology · 2015Review
- Treatment of experimental stroke with IL-10-producing B-cells reduces infarct size and peripheral and CNS inflammation in wild-type B-cell-sufficient mice.Metabolic brain disease · 2014Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Oestrogen (17β-oestradiol, E₂) is a highly effective treatment for experimental autoimmune encephalomyelitis (EAE) that may potentiate Foxp3+ regulatory T (Treg) cells, which in turn limit the expansion of encephalitogenic T-cell specificities. To determine if Treg cells constitute the major non-redundant protective pathway for E₂, we evaluated E₂ protection of EAE after targeted deletion of Foxp3 expression in Foxp3-DTR mice. Unexpectedly, E₂-treated Foxp3-deficient mice were completely protected against clinical and histological myelin oligodendrocyte glycoprotein (MOG)-35-55 peptide-induced EAE before succumbing to diphtheria toxin-induced mortality. This finding indicated the presence of alternative E₂-dependent EAE-protective pathways that could compensate for the lack of Treg cells. Further investigation revealed that E₂ treatment inhibited proliferation and expression of CCL2 and CXCL2, but enhanced secretion of interleukin-10 (IL-10) and IL-13 by MOG-35-55-specific spleen cells. These changes occurred concomitantly with increased expression of several chemokines and receptors, including CXCL13 and CXCR5, and the negative co-activation molecules, PD-L1 and B7.2, by B cells and dendritic cells. Furthermore, E₂ treatment resulted in higher percentages of spleen and lymph node T cells expressing IL-17, interferon-γ and tumour necrosis factor-α, but with lower expression of CCR6, suggesting sequestration of MOG-35-55 peptide-specific T cells in peripheral immune organs. Taken together, these data suggest that E₂-induced mechanisms that provide protection against EAE in the absence of Foxp3+ Treg cells include induction of regulatory B cells and peripheral sequestration of encephalitogenic T cells.
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Registered trials
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