IL-17 receptor signaling and T helper 17-mediated autoimmune demyelinating disease

被引：196

作者：

Zepp, Jarod ^{[1
,2
]}

Wu, Ling ^{[1
,3
]}

Li, Xiaoxia ^{[1
]}

机构：

[1] Cleveland Clin, Dept Immunol, Cleveland, OH 44195 USA

[2] Case Western Reserve Univ, Dept Mol Med, Cleveland, OH 44106 USA

[3] Case Western Reserve Univ, Dept Pathol, Cleveland, OH 44106 USA

来源：

TRENDS IN IMMUNOLOGY | 2011年 / 32卷 / 05期

关键词：

GENOME-WIDE ASSOCIATION; NECROSIS-FACTOR-ALPHA; MULTIPLE-SCLEROSIS; ADAPTER PROTEIN; ANIMAL-MODELS; TH17; CELLS; INTERLEUKIN-17; ACT1; EXPRESSION; CYTOKINE;

D O I：

10.1016/j.it.2011.02.007

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). Experimental autoimmune encephalomyelitis (EAE) is widely used to dissect molecular mechanisms of MS and to develop new therapeutic strategies. The T helper 17 (Th17) subset of CD4 T cells plays a crucial role in the development of EAE. IL-17, a cytokine produced by Th17 cells, participates in EAE pathogenesis through induction of inflammatory gene expression in target cells. Recent work has shown that Act1, a U-box E3 ubiquitin ligase, is recruited to IL-17 receptor (IL-17R) upon IL-17 stimulation and is required for IL-17-mediated signaling. Here, we review the molecular and cellular mechanisms by which IL-17 and Act1-mediated signaling contribute to EAE.

引用

页码：232 / 239

页数：8

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