Transcriptional regulation of Th17 cell differentiation

被引：508

作者：

Ivanov, Ivaylo I. ^{[1
]}

Zhou, Liang ^{[1
]}

Littman, Dan R. ^{[1
,2
]}

机构：

[1] NYU, Sch Med, Skirball Inst Biomol Med, Kimmel Ctr Biol & Med, New York, NY 10016 USA

[2] Howard Hughes Med Inst, New York, NY 10016 USA

来源：

SEMINARS IN IMMUNOLOGY | 2007年 / 19卷 / 06期

关键词：

Th17; IL-17; ROR gamma t; mucosal immunity; regulatory T cells;

D O I：

10.1016/j.smim.2007.10.011

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 [免疫学];

摘要：

The paradigm of effector T helper cell differentiation into either Th1 or Th2 lineages has been profoundly shaken by the discovery of T cells that secrete IL-17 and other inflammatory cytokines. This subset, referred to as Th17, is centrally involved in autoimmune disease and is important in host defense at mucosal surfaces. In mouse, a series of cytokines, including IL-6, IL-21, IL-23, and TGF-beta, function sequentially or synergistically to induce the Th17 lineage. Other cytokines, including IL-2, IL-4, IFN gamma, and IL-27, inhibit differentiation of this lineage. Here we review how the nuclear orphan receptor ROR gamma t functions to coordinate the diverse cytokine-induced signals and thus controls Th17 cell differentiation. (C) 2007 Elsevier Ltd. All rights reserved.

引用

页码：409 / 417

页数：9

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