免疫系统
生物
人口
RAR相关孤儿受体γ
促炎细胞因子
转录因子
细菌
免疫
微生物学
炎症
免疫学
肠道菌群
细胞生物学
FOXP3型
基因
遗传学
医学
环境卫生
作者
Caspar Ohnmacht,Joo-Hong Park,Sascha Cording,James B. Wing,Koji Atarashi,Yuuki Obata,Valérie Gaboriau‐Routhiau,Rute Marques,Sophie Dulauroy,Maria Fedoseeva,Meinrad Busslinger,Nadine Cerf–Bensussan,Ivo G. Boneca,David Voehringer,Koji Hase,Kenya Honda,Shimon Sakaguchi,Gérard Eberl
出处
期刊:Science
[American Association for the Advancement of Science]
日期:2015-07-09
卷期号:349 (6251): 989-993
被引量:865
标识
DOI:10.1126/science.aac4263
摘要
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.
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