Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid

被引:1588
作者
Mucida, Daniel [1 ]
Park, Yunji [1 ]
Kim, Gisen [1 ]
Turovskaya, Olga [1 ]
Scott, Iain [1 ]
Kronenberg, Mitchell [1 ]
Cheroutre, Hilde [1 ]
机构
[1] La Jolla Inst Allergy & Immunol, La Jolla, CA 92037 USA
关键词
TGF-BETA; INFLAMMATION; GENERATION; FOXP3;
D O I
10.1126/science.1145697
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
The cytokine transforming growth factor-beta (TGF-beta) converts naive 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 naive T lymphocytes into proinflammatory IL-17 cytokine-producing T helper 17 (TH17) 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 TH17 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.
引用
收藏
页码:256 / 260
页数:5
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