Interleukin-6 as a key player in systemic inflammation and joint destruction
Interleukin-6 as a key player in systemic inflammation and joint destruction
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DOI：
10.1016/j.autrev.2009.01.012
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发表时间：
2009-06-01
影响因子：
13.6
通讯作者：
Choy, E.
中科院分区：
文献类型：
--
作者：
Fonseca, J. E.;Santos, M. J.;Choy, E.
白细胞介素-6（IL-6）是一种细胞因子，可以促进自身免疫现象，放大急性炎症并促进演变为慢性炎症状态。此外，它是病理条件下骨吸收的主要促进剂。特别地，IL-6在滑膜炎、骨侵蚀和炎症的全身特征中具有关键作用。该细胞因子特异性结合IL-6受体（IL-6 R），形成IL-6/IL-6 R复合物，与gp 130（一种膜结合蛋白，参与非配体结合信号转导）结合。用人源化抗IL-6 R单克隆抗体（托珠单抗）在关节炎动物模型和类风湿性关节炎患者中靶向IL-6 R，可有效控制局部和全身炎症表现，并阻断软骨和骨破坏。鉴于IL-6的多效性功能，可以预期其他炎性疾病和骨代谢病症可能受益于选择性IL-6信号传导抑制。(C)2009 Elsevier B. V.保留所有权利。
Interleukin-6 (IL-6) is a cytokine that can facilitate autoimmune phenomena, amplify acute inflammation and promote the evolution into a chronic inflammatory state. In addition, it is a major promoter of bone resorption in pathological conditions. In particular, IL-6 has a pivotal role in synovitis, bone erosions and in the systemic features of inflammation. This cytokine specifically binds to IL-6 receptor (IL-6R), forming the IL-6/IL-6R complex that binds to gp130, a membrane-bound protein, which is involved in non-ligand-binding signal transduction. Targeting IL-6R in both animal models of arthritis and in rheumatoid arthritis patients with a humanized anti IL-6R monoclonal antibody (tocilizumab) effectively controls local and systemic inflammatory manifestations and blocks cartilage and bone destruction. Given the pleiotropic function of IL-6 it can be anticipated that other inflammatory diseases and bone metabolic conditions might benefit from selective IL-6 signaling inhibition. (C) 2009 Elsevier B.V. All rights reserved.