| Literature DB >> 26160380 |
Caspar Ohnmacht1, Joo-Hong Park1, Sascha Cording1, James B Wing2, Koji Atarashi3, Yuuki Obata4, Valérie Gaboriau-Routhiau5, Rute Marques1, Sophie Dulauroy1, Maria Fedoseeva6, Meinrad Busslinger7, Nadine Cerf-Bensussan8, Ivo G Boneca9, David Voehringer10, Koji Hase4, Kenya Honda11, Shimon Sakaguchi12, Gérard Eberl13.
Abstract
Changes to the symbiotic microbiota early in life, or the absence of it, can lead to exacerbated type 2 immunity and allergic inflammations. Although it is unclear how the microbiota regulates type 2 immunity, it is a strong inducer of proinflammatory T helper 17 (T(H)17) cells and regulatory T cells (T(regs)) in the intestine. Here, we report that microbiota-induced T(regs) express the nuclear hormone receptor RORγt and differentiate along a pathway that also leads to T(H)17 cells. In the absence of RORγt(+) T(regs), T(H)2-driven defense against helminths is more efficient, whereas T(H)2-associated pathology is exacerbated. Thus, the microbiota regulates type 2 responses through the induction of type 3 RORγt(+) T(regs) and T(H)17 cells and acts as a key factor in balancing immune responses at mucosal surfaces.Entities:
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Year: 2015 PMID: 26160380 DOI: 10.1126/science.aac4263
Source DB: PubMed Journal: Science ISSN: 0036-8075 Impact factor: 47.728