从饮食到细胞核：维生素A与转化生长因子-β在肠道黏膜界面协同作用。
From the diet to the nucleus: vitamin A and TGF-beta join efforts at the mucosal interface of the intestine.
作者信息
Mucida Daniel, Park Yunji, Cheroutre Hilde
机构信息
La Jolla Institute for Allergy and Immunology, 9420 Athena Circle, La Jolla, CA 92037, USA.
出版信息
Semin Immunol. 2009 Feb;21(1):14-21. doi: 10.1016/j.smim.2008.08.001. Epub 2008 Sep 21.
Abstract
The vitamin A metabolites, including retinoic acid (RA), form ligands for retinoic acid-related nuclear receptors and together they play pleiotropic roles in various biological processes. Recently, we described that RA also functions as a key modulator of transforming growth factor-beta (TGF-beta)-driven immune deviation, capable of suppressing the differentiation of interleukin-17 secreting T helper cells (T(H)17) and conversely promoting the generation of Foxp3(+) T regulatory (Treg) cells. This review will focus on the role of RA in the reciprocal TGF-beta-driven differentiation of T(H)17 and Treg and on the importance of such regulatory mechanism to control a functional immune system, in particular at the mucosal interface of the intestine.
摘要
维生素A代谢产物，包括视黄酸（RA），可形成视黄酸相关核受体的配体，它们共同在各种生物学过程中发挥多效性作用。最近，我们描述了RA还是转化生长因子-β（TGF-β）驱动的免疫偏离的关键调节因子，能够抑制分泌白细胞介素-17的辅助性T细胞（Th17）的分化，反之促进Foxp3（+）调节性T细胞（Treg）的生成。本综述将聚焦于RA在TGF-β驱动的Th17和Treg相互分化中的作用，以及这种调节机制对于控制功能性免疫系统，特别是在肠道黏膜界面的重要性。
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