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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.

DOI:10.1016/j.smim.2008.08.001
PMID:18809338
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2643336/
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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本文引用的文献

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Adaptive Foxp3+ regulatory T cell-dependent and -independent control of allergic inflammation.适应性Foxp3 +调节性T细胞依赖性和非依赖性对变应性炎症的控制
Immunity. 2008 Jul 18;29(1):114-26. doi: 10.1016/j.immuni.2008.05.010.
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Molecular antagonism and plasticity of regulatory and inflammatory T cell programs.调节性和炎性T细胞程序的分子拮抗作用与可塑性
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Regulation of humoral and cellular gut immunity by lamina propria dendritic cells expressing Toll-like receptor 5.表达Toll样受体5的固有层树突状细胞对肠道体液免疫和细胞免疫的调节
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Cytokines secreted in response to Toll-like receptor ligand stimulation modulate differentiation of human Th17 cells.响应Toll样受体配体刺激而分泌的细胞因子可调节人Th17细胞的分化。
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A critical function for TGF-beta signaling in the development of natural CD4+CD25+Foxp3+ regulatory T cells.转化生长因子β信号在天然CD4+CD25+Foxp3+调节性T细胞发育中的关键作用。
Nat Immunol. 2008 Jun;9(6):632-40. doi: 10.1038/ni.1607. Epub 2008 Apr 27.
6
Foxp3 inhibits RORgammat-mediated IL-17A mRNA transcription through direct interaction with RORgammat.Foxp3通过与RORγt直接相互作用来抑制RORγt介导的IL-17A mRNA转录。
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7
STAT6 Inhibits TGF-beta1-mediated Foxp3 induction through direct binding to the Foxp3 promoter, which is reverted by retinoic acid receptor.信号转导及转录激活因子6(STAT6)通过直接结合叉头框蛋白3(Foxp3)启动子来抑制转化生长因子-β1(TGF-β1)介导的Foxp3诱导,而视黄酸受体可逆转这种抑制作用。
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8
TGF-beta-induced Foxp3 inhibits T(H)17 cell differentiation by antagonizing RORgammat function.转化生长因子β诱导的Foxp3通过拮抗RORγt功能抑制辅助性T细胞17分化。
Nature. 2008 May 8;453(7192):236-40. doi: 10.1038/nature06878. Epub 2008 Mar 26.
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Blood. 2008 Feb 1;111(3):1013-20. doi: 10.1182/blood-2007-06-096438. Epub 2007 Oct 19.