促炎细胞因子
维甲酸
自身免疫
调节性T细胞
细胞生物学
炎症
细胞因子
T细胞
免疫系统
免疫学
白细胞介素17
生物
调节器
化学
FOXP3型
白细胞介素2受体
生物化学
细胞培养
遗传学
基因
作者
Daniel Mucida,Yunji Park,Gisen Kim,Olga Turovskaya,Iain Scott,Mitchell Kronenberg,Hilde Cheroutre
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2007-07-13
卷期号:317 (5835): 256-260
被引量:1801
标识
DOI:10.1126/science.1145697
摘要
The cytokine transforming growth factor-beta (TGF-beta) converts naïve T cells into regulatory T (Treg) cells that prevent autoimmunity. However, in the presence of interleukin-6 (IL-6), TGF-beta has also been found to promote the differentiation of naïve T lymphocytes into proinflammatory IL-17 cytokine-producing T helper 17 (T(H)17) cells, which promote autoimmunity and inflammation. This raises the question of how TGF-beta can generate such distinct outcomes. We identified the vitamin A metabolite retinoic acid as a key regulator of TGF-beta-dependent immune responses, capable of inhibiting the IL-6-driven induction of proinflammatory T(H)17 cells and promoting anti-inflammatory Treg cell differentiation. These findings indicate that a common metabolite can regulate the balance between pro- and anti-inflammatory immunity.
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