TGFβ and Retinoic Acid Intersect in Immune-Regulation

被引:46
作者
Mucida, Daniel [1 ]
Cheroutre, Hilde [1 ]
机构
[1] La Jolla Inst Allergy & Immunol, La Jolla, CA 92037 USA
关键词
TGF beta; retinoic acid; Foxp3; TH17; IL-6; mucosal immune regulation; oral tolerance; transcription factors;
D O I
10.4161/cam.1.3.5062
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Transforming growth factor (TGF beta) prevents T(H)1 and T(H)2 differentiation and converts naive CD4 cells into Foxp3-expressing T regulatory (Treg) cell.(1,2) In sharp contrast, in the presence of pro-inflammatory cytokines, including IL-6, TGF beta not only inhibits Foxp3 expression but also promotes the differentiation of pro-inflammatory IL17-producing CD4 effector T (T(H)17) cells.(3-5) This reciprocal TGF beta-dependent differentiation imposes a critical dilemma between pro- and anti-inflammatory immunity and suggests that a sensitive regulatory mechanism must exist to control TGF beta-driven T(H)17 effector and Treg differentiation. A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGF beta-driven-immune deviation capable of suppressing T(H)17 differentiation while promoting Foxp3(+) Treg generation.(6-10)
引用
收藏
页码:142 / 144
页数:3
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