转化生长因子β（TGFβ）与视黄酸在免疫调节中相互作用。
TGFbeta and retinoic acid intersect in immune-regulation.
作者信息
Mucida Daniel, Cheroutre Hilde
机构信息
La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.
出版信息
Cell Adh Migr. 2007 Jul-Sep;1(3):142-4. doi: 10.4161/cam.1.3.5062. Epub 2007 Jul 20.
Abstract
Transforming growth factor (TGFbeta) prevents T(H)1 and T(H)2 differentiation and converts naïve CD4 cells into Foxp3-expressing T regulatory (Treg) cell.(1,2) In sharp contrast, in the presence of pro-inflammatory cytokines, including IL-6, TGFbeta 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 TGFbeta-dependent differentiation imposes a critical dilemma between pro- and anti-inflammatory immunity and suggests that a sensitive regulatory mechanism must exist to control TGFbeta-driven T(H)17 effector and Treg differentiation. A vitamin A metabolite, retinoic acid (RA), was recently identified as a key modulator of TGFbeta-driven- immune deviation capable of suppressing T(H)17 differentiation while promoting Foxp3(+)Treg generation.(6-10).
摘要
转化生长因子（TGFβ）可阻止辅助性T细胞1（TH1）和辅助性T细胞2（TH2）分化，并将初始CD4细胞转化为表达叉头框蛋白3（Foxp3）的调节性T（Treg）细胞。（1,2）与之形成鲜明对比的是，在包括白细胞介素6（IL-6）在内的促炎细胞因子存在的情况下，TGFβ不仅会抑制Foxp3表达，还会促进产生促炎白细胞介素17的CD4效应T（TH17）细胞的分化。（3-5）这种相互的依赖TGFβ的分化在促炎和抗炎免疫之间造成了一个关键困境，并表明必须存在一种敏感的调节机制来控制TGFβ驱动的TH17效应细胞和Treg分化。一种维生素A代谢产物，视黄酸（RA），最近被确定为TGFβ驱动的免疫偏向的关键调节因子，它能够抑制TH17分化，同时促进Foxp3（+）Treg的产生。（6-10）
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本文引用的文献
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