期刊
CELL ADHESION & MIGRATION
卷 1, 期 3, 页码 142-144出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/cam.1.3.5062
关键词
TGF beta; retinoic acid; Foxp3; TH17; IL-6; mucosal immune regulation; oral tolerance; transcription factors
类别
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)
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