Therapeutic strategies for the clinical blockade of IL-6/gp130 signaling

被引：575

作者：

Jones, Simon A. ^{[2
]}

Scheller, Juergen ^{[3
]}

Rose-John, Stefan ^{[1
]}

机构：

[1] Univ Kiel, Inst Biochem, D-24098 Kiel, Germany

[2] Cardiff Univ, Sch Med, Dept Infect Immun & Biochem, Cardiff, S Glam, Wales

[3] Univ Dusseldorf, Fac Med, Inst Biochem & Mol Biol 2, Dusseldorf, Germany

来源：

JOURNAL OF CLINICAL INVESTIGATION | 2011年 / 121卷 / 09期

基金：

英国惠康基金;

关键词：

SOLUBLE IL-6 RECEPTOR; LEUKEMIA INHIBITORY FACTOR; TUMOR-NECROSIS-FACTOR; RHEUMATOID-ARTHRITIS; INTERLEUKIN-6; RECEPTOR; ONCOSTATIN-M; TGF-BETA; ANTIINFLAMMATORY CYTOKINE; HEPATIC INFLAMMATION; EXPERIMENTAL-MODEL;

D O I：

10.1172/JCI57158

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

The successful treatment of certain autoimmune conditions with the humanized anti-IL-6 receptor (IL-6R) antibody tocilizumab has emphasized the clinical importance of cytokines that signal through the beta-receptor subunit glycoprotein 130 (gp130). In this Review, we explore how gp130 signaling controls disease progression and examine why IL-6 has a special role among these cytokines as an inflammatory regulator. Attention will be given to the role of the soluble IL-6R, and we will provide a perspective into the clinical blockade of IL-6 activity in autoimmunity, inflammation, and cancer.

引用

页码：3375 / 3383

页数：9

共 129 条

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