IL-6 in autoimmune disease and chronic inflammatory proliferative disease

被引:666
作者
Ishihara, K
Hirano, T
机构
[1] Osaka Univ, Grad Sch Med, Dept Mol Oncol C7, Suita, Osaka 5650871, Japan
[2] Osaka Univ, Grad Sch Frontier Biosci, Lab Dev Immunol, Suita, Osaka 5650871, Japan
[3] RIKEN, Res Ctr Allergy & Immunol, Lab Cytokine Signaling, Kanagawa, Japan
关键词
interleukin; 6; signal transduction; autoimmune disease; chronic inflammatory proliferative disease (CIPD);
D O I
10.1016/S1359-6101(02)00027-8
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Interleukin 6 (IL-6), which was originally identified as a B-cell differentiation factor, is now known to be a multifunctional cytokine that regulates the immune response, hematopoiesis, the acute phase response, and inflammation. Deregulation of IL-6 production is implicated in the pathology of several disease processes. The expression of constitutively high levels of IL-6 in transgenic mice results in fatal plasmacytosis, which has been implicated in human multiple myeloma. Increased IL-6 levels are also observed in several diseases, including rheumatoid arthritis (RA), systemic-onset juvenile chronic arthritis (JCA), osteoporosis, and psoriasis. IL-6 is critically involved in experimentally induced autoimmune disease, such as antigen-induced arthritis (AIA), and experimental allergic encephalomyelitis. All these clinical data and animal models suggest that IL-6 plays critical roles in the pathogenesis of autoimmune diseases. Here we review the evidence for the involvement of IL-6 in the pathophysiology of autoimmune diseases and chronic inflammatory proliferative diseases (CIPD) and discuss the possible molecular mechanisms of its involvement. (C) 2002 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码:357 / 368
页数:12
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