IL-33: a promising therapeutic target for rheumatoid arthritis?

被引:57
作者
Yuan, Feng-Lai [1 ]
Li, Xia [1 ]
Lu, Wei-Guo [1 ]
Li, Cheng-Wan [1 ]
Xu, Rui-Sheng [1 ]
Dong, Jian [2 ]
机构
[1] Nantong Univ, Hosp Affiliated 3, Wuxi 214041, Jiangsu, Peoples R China
[2] Fudan Univ, Dept Orthopaed Surg, Zhongshan Hosp, Shanghai 200032, Peoples R China
基金
美国国家科学基金会;
关键词
RECEPTOR ACCESSORY PROTEIN; COLLAGEN-INDUCED ARTHRITIS; MAST-CELLS; CARTILAGE DESTRUCTION; SYNOVIAL FIBROBLASTS; JOINT INFLAMMATION; GENE-EXPRESSION; CYTOKINE IL-33; BONE EROSION; NK CELLS;
D O I
10.1517/14728222.2011.560838
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
Cytokine-mediated immunity plays a crucial role in the pathogenesis of various autoimmune diseases, including rheumatoid arthritis (RA). Recently, the IL-1-family-related cytokine, IL-33, was detected at high levels in experimental inflammatory arthritis and in the early phase of human RA, and was reported to exert profound pro-inflammatory effects in several experimental autoimmune models. Moreover, administration of IL-33 leads to the development of severe inflammatory arthritis, suggesting that IL-33 may be therapeutically relevant in RA, and the targeting of IL-33 or the IL-33 receptor has been proposed as a potential therapeutic approach for autoimmune diseases such as RA. In this article, we discuss the biological features of IL-33 and summarize recent advances in our understanding of the role of IL-33 in the pathogenesis and treatment of RA. It is hoped that this information may aid the development of novel therapeutic strategies for RA.</.
引用
收藏
页码:529 / 534
页数:6
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