Engler, Jan Broder;
Kursawe, Nina;
Solano, María Emilia;
Patas, Kostas;
Wehrmann, Sabine;
Heckmann, Nina;
Lühder, Fred;
Reichardt, Holger M.;
Arck, Petra Clara;
Gold, Stefan M.;
Friese, Manuel A.
Glucocorticoid receptor in T cells mediates protection from autoimmunity in pregnancy
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Medientyp:
E-Artikel
Titel:
Glucocorticoid receptor in T cells mediates protection from autoimmunity in pregnancy
Beteiligte:
Engler, Jan Broder;
Kursawe, Nina;
Solano, María Emilia;
Patas, Kostas;
Wehrmann, Sabine;
Heckmann, Nina;
Lühder, Fred;
Reichardt, Holger M.;
Arck, Petra Clara;
Gold, Stefan M.;
Friese, Manuel A.
Erschienen:
National Academy of Sciences, 2017
Erschienen in:
Proceedings of the National Academy of Sciences of the United States of America, 114 (2017) 2, Seite E181-E190
Sprache:
Englisch
ISSN:
1091-6490;
0027-8424
Entstehung:
Anmerkungen:
Beschreibung:
Pregnancy is one of the strongest inducers of immunological tolerance. Disease activity of many autoimmune diseases including multiple sclerosis (MS) is temporarily suppressed by pregnancy, but little is known about the underlying molecular mechanisms. Here, we investigated the endocrine regulation of conventional and regulatory T cells (Tregs) during reproduction. In vitro, we found the pregnancy hormone progesterone to robustly increase Treg frequencies via promiscuous binding to the glucocorticoid receptor (GR) in T cells. In vivo, T-cell–specific GR deletion in pregnant animals undergoing experimental autoimmune encephalomyelitis (EAE), the animal model of MS, resulted in a reduced Treg increase and a selective loss of pregnancy-induced protection, whereas reproductive success was unaffected. Our data imply that steroid hormones can shift the immunological balance in favor of Tregs via differential engagement of the GR in T cells. This newly defined mechanism confers protection from autoimmunity during pregnancy and represents a potential target for future therapy.