Rheumatoid Arthritis and Tumor Necrosis Factor α

Rheumatoid Arthritis and Tumor Necrosis Factor α
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类风湿关节炎与肿瘤坏死因子α

DOI:
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发表时间:
2001
期刊:
影响因子:
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通讯作者:
T. Takeuchi
T. Takeuchi
中科院分区:
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文献类型:
--
作者:
T. Abe;T. Takeuchi

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类风湿性关节炎(RA)是一种病因不明的慢性破坏性和变形性关节炎。类风湿炎症始于滑膜,以新生血管、单核细胞浸润和滑膜细胞增生为特征。滑膜因滑膜细胞和炎症细胞浸润而增厚。这些细胞导致炎症形成,侵入并破坏关节软骨和骨骼。RA的传统范式已经揭示了多种促成滑膜炎症起始和延续的机制,包括T细胞活化、细胞因子网络的形成和持续以及细胞毒性分子的产生。本文首先介绍了我们对RA发病机制的了解,然后重点介绍了tnf的作用。
Rheumatoid arthritis (RA) is a chronic destructive and deforming arthritis of unknown etiology. Rheumatoid inflammation starts in the synovial membrane and is characterized by neovascularization, mononuclear cell infiltration, and synovial cell proliferation. The synovial membrane becomes thickened by synovial cell and inflammatory cell infiltration. These cells lead to the formation of an inflamed pannus, which invades and destroys articular cartilage and bone. The traditional paradigm of RA has disclosed a variety of mechanisms that contribute to the initiation and perpetuation of synovial inflammation, including T cell activation, the formation and persistence of a cytokine network, and production of cytotoxic molecules. This review first describes what we have learned about the pathogenesis of RA and then focuses on the role of TNF.a.
DOI: 10.1016/s1074-7613(00)80038-2
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期刊: IMMUNITY
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