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Ohnmacht, C. ; Park, J.H.* ; Cording, S.* ; Wing, J.B.* ; Atarashi, K.* ; Obata, Y.* ; Gaboriau-Routhiau, V.* ; Marques, R.* ; Dulauroy, S.* ; Fedoseeva, M. ; Busslinger, M.* ; Cerf-Bensussan, N.* ; Boneca, I.G.* ; Voehringer, D.* ; Hase, K.* ; Honda, K.* ; Sakaguchi, S.* ; Eberl, G.*

The microbiota regulates type 2 immunity through RORγt+ T cells.

Science 349, 989-993 (2015)
DOI PMC
Open Access Green as soon as Postprint is submitted to ZB.
Changes to the symbiotic microbiota early in life, or the absence of it, can lead to exacerbated type 2 immunity and allergic inflammations. While it is unclear how the microbiota regulates type 2 immunity, it is a strong inducer of pro-inflammatory T helper (Th) 17 cells and regulatory T cells (Tregs) in the intestine. Here, we report that microbiota-induced Tregs express the nuclear hormone receptor RORγt and differentiate along a pathway that also leads to Th17 cells. In the absence of RORγt(+) Tregs, Th2-driven defense against helminths is more efficient while Th2-associated pathology is exacerbated. Thus, the microbiota regulates type 2 responses through the induction of "type 3" RORγt(+) Tregs and Th17 cells and acts as a key factor in balancing immune responses at mucosal surfaces.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Ror-gamma-t; Innate Lymphoid-cells; Early-life; Proinflammatory Il-17(+); Commensal Bacteria; Oxazolone Colitis; Helper-cells; Differentiation; Inflammation; Susceptibility
ISSN (print) / ISBN 0036-8075
e-ISSN 1095-9203
Journal Science
Quellenangaben Volume: 349, Issue: 6251, Pages: 989-993 Article Number: , Supplement: ,
Publisher American Association for the Advancement of Science (AAAS)
Publishing Place Washington
Non-patent literature Publications
Reviewing status Peer reviewed
Institute(s) Institute for Allergy Research (IAF)