Type II collagen autoimmunity in a mouse model of human rheumatoid arthritis

被引：194

作者：

Cho, Young-Gyu

Cho, Mi-La

Min, So-Youn

Kim, Ho-Youn

机构：

[1] Catholic Univ Korea, Sch Med, Kang Nam St Marys Hosp, Rheumatism Res Ctr, Seoul 137701, South Korea

[2] Catholic Univ Korea, Sch Med, Dept Internal Med, Div Rheumatol, Seoul 137701, South Korea

[3] Catholic Univ Korea, Ctr Rheumatoid Dis, Dept Med, Div Rheumatol, Seoul, South Korea

[4] Catholic Univ Korea, Rheumatism Res Ctr, Catholic Res Inst Med Sci, Seoul, South Korea

来源：

AUTOIMMUNITY REVIEWS | 2007年 / 7卷 / 01期

关键词：

rheumatoid arthritis (RA); collagen-induced arthritis (CIA); IL-17; toll-like receptor (TLR);

D O I：

10.1016/j.autrev.2007.08.001

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Type II collagen (CII) is expressed exclusively in the joint articular. Although the relationship between anti-CII immunity and human rheumatoid arthritis (RA) has been studied for a long time, definitive conclusions have not been reached. CII, as an autoantigen, has been studied extensively in small animal models, such as mice, and the collagen-induced arthritis (CIA) model has increased our understanding of the pathogenesis of human RA. In the present report, we summarize the available information on anti-CII immunity and discuss recent updates regarding pathogenesis in the CIA model, including the role of Th17 cells. (c) 2007 Elsevier B.V. All rights reserved.

引用

页码：65 / 70

页数：6

共 41 条

[1] IL-4 abrogates osteoclastogenesis through STAT6-dependent inhibition of NF-κB [J].