Evidence for the role of Th17 cell inhibition in the prevention of autoimmune diseases by anti-interluekin-6 receptor antibody

被引：28

作者：

Mihara, Masahiko ^{[1
]}

Ohsugi, Yoshiyuki ^{[1
]}

Kishimoto, Tadamitsu ^{[2
]}

机构：

[1] Chugai Pharmaceut Co Ltd, Prod Res Dept, Fuji Gotemba Res Labs, Gotemba, Shizuoka 4128513, Japan

[2] Osaka Univ, Lab Immune Regulat, Grad Sch Frontier Biosci, Suita, Osaka 565, Japan

来源：

BIOFACTORS | 2009年 / 35卷 / 01期

关键词：

Anti-IL-6R antibody; rheumatoid arthritis; Th-17; Th-1; COLLAGEN-INDUCED ARTHRITIS; GROWTH-FACTOR-BETA; TYPE-1; T-HELPER; RHEUMATOID-ARTHRITIS; TH17; CELLS; DOUBLE-BLIND; INTERLEUKIN-6; GAMMA; INDUCTION; MICE;

D O I：

10.1002/biof.9

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Deregulated production of interleukin-6 (IL-6) has been found in several chronic inflammatory autoimmune disorders, including rheumatoid arthritis (RA) and inflammatory bowel diseases. Treatment with tocilizumab, a humanized antihuman IL-6 receptor (IL-6R) antibody, significantly proved disease activity and inhibited the progression of joint destruction in RA patients, but the reason why IL-6 blockade causes improvement of RA is still unclear. In this review, we discuss the influence of anti-IL-6R antibody treatment on the differentiation of Th-17 cells, which are thought to be involved in the pathogenesis of autoimmune diseases in animal models, present new results for the effect of anti-IL-6R antibody on the induction of Th-17 cells in a mouse collagen-induced arthritis model, and come to the conclusion that anti-IL-6R antibody inhibited the differentiation of Th-17 cells in mouse models. It is thought that this inhibitory action may contribute to the therapeutic effects of anti-IL-6R antibody in human autoimmune diseases. (C) 2009 international Union of Biochemistry and Molecular Biology, Inc. Volume 35, Number 1, January/February 2009, Pages 47-51. E-mail: miharamsh@chugai-pharm.co.jp

引用

页码：47 / 51

页数：5

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