Event Abstract Back to Event Cell-intrinsic estrogen receptor α activation in CD4+ T cells control Th1/Th17 differentiation in trans and protect from CNS autoimmunity Sophie LAFFONT1*, Laure Garnier1, Nelly Rouquie1 and Jean-Charles Guéry1 1 Centre de Physiopathologie de Toulouse Purpan - Inserm U1043, France Estrogens influence many physiological processes in mammals. In autoimmune diseases, estrogens can display either beneficial or deleterious effects. Clinical remissions in patients with multiple sclerosis (MS) during pregnancy have suggested that sex hormones, particularly estrogens, could modulate CNS-autoimmunity and inflammation. Indeed, 17ß-estradiol (E2) treatment has been shown to inhibit the development of experimental autoimmune encephalomyelitis (EAE), the animal model of (MS). Two molecular targets essentially mediate E2 actions: estrogen receptor alpha (ERα) and beta (ERβ). We and others have shown that the protective effect of E2 on EAE was strictly dependent on ERα. However, the underlying mechanisms responsible of anti-inflammatory effect of E2 in EAE protection are still ill defined. Using tissue-specific ERαKO mouse models, we demonstrated that ERα-signaling in T lymphocytes, but not myeloid cells (monocytes/macrophages or dendritic cells), was required for sustained EAE protection by E2 (Lélu et al., J. Immunol. 2011 187:2386). Using adoptive transfer model of MOG-specific 2D2 CD4 T cells, we now show that ERα-signaling in endogenous host CD4+ T lymphocytes rather than responding 2D2 CD4+ T cells orchestrates the inhibition of MOG-specific Th1/Th17 cell priming. Coadministration of naive 2D2 ERα-/- T cells with E2-responsive ERα+/+, but not ERα-/-, CD4 T cells strongly delayed EAE development in Rag2-/- ERα-/- hosts. Thus, these results identify a suppressive activity of E2-primed CD4+ T cells, by which they can restrict differentiation of Th17 cells in trans and protect from CNS autoimmunity. Keywords: Estradiol, Estrogen Receptor alpha, CD4-Positive T-Lymphocytes, Th17, Th1 Cells, Encephalomyelitis, Autoimmune, Experimental, Central Nervous System Conference: 15th International Congress of Immunology (ICI), Milan, Italy, 22 Aug - 27 Aug, 2013. Presentation Type: Abstract Topic: Immune-mediated disease pathogenesis Citation: LAFFONT S, Garnier L, Rouquie N and Guéry J (2013). Cell-intrinsic estrogen receptor α activation in CD4+ T cells control Th1/Th17 differentiation in trans and protect from CNS autoimmunity. Front. Immunol. Conference Abstract: 15th International Congress of Immunology (ICI). doi: 10.3389/conf.fimmu.2013.02.00952 Copyright: The abstracts in this collection have not been subject to any Frontiers peer review or checks, and are not endorsed by Frontiers. They are made available through the Frontiers publishing platform as a service to conference organizers and presenters. The copyright in the individual abstracts is owned by the author of each abstract or his/her employer unless otherwise stated. Each abstract, as well as the collection of abstracts, are published under a Creative Commons CC-BY 4.0 (attribution) licence (https://creativecommons.org/licenses/by/4.0/) and may thus be reproduced, translated, adapted and be the subject of derivative works provided the authors and Frontiers are attributed. For Frontiers’ terms and conditions please see https://www.frontiersin.org/legal/terms-and-conditions. Received: 28 Jun 2013; Published Online: 22 Aug 2013. * Correspondence: Dr. Sophie LAFFONT, Centre de Physiopathologie de Toulouse Purpan - Inserm U1043, Toulouse, France, sophie.laffont-pradines@inserm.fr Login Required This action requires you to be registered with Frontiers and logged in. To register or login click here. Abstract Info Abstract The Authors in Frontiers Sophie LAFFONT Laure Garnier Nelly Rouquie Jean-Charles Guéry Google Sophie LAFFONT Laure Garnier Nelly Rouquie Jean-Charles Guéry Google Scholar Sophie LAFFONT Laure Garnier Nelly Rouquie Jean-Charles Guéry PubMed Sophie LAFFONT Laure Garnier Nelly Rouquie Jean-Charles Guéry Related Article in Frontiers Google Scholar PubMed Abstract Close Back to top Javascript is disabled. Please enable Javascript in your browser settings in order to see all the content on this page.