| 英文摘要 |
Rheumatoid arthritis (RA) is a chronic inflammatory disease characterized with polyarticular involvement, which often results in joint deformity and disability in cases with poor control. Though lots of medications including DMARDs and biologic agents have been developed, there is no cure to date. Therefore, a further investigation upon the pathogenesis of RA is mandatory. Recently, a critical molecular, fractalkine has been found to be a critical molecule in the pathogenesis of RA. Activated fibroblast-like synoviocytes (FLS) express lots of fractalkine molecules, which attract CD4+CD28–CX3CR1+ T cells to be closely contacted. Thereafter, activated FLS works as an antigen presenting cell to send costimulatory signals to stimulate CD4+CD28–CX3CR1+ T cells, which then releasing lots of proinflammatory cytokines to cause proliferation of FLS. In addition, fractalkine is also known as an important angiogenetic factors to cause neovascularization in RA synovium. Furthermore, biologic agents to block fractalkine activity have been found to be able to attenuate the synovial inflammation in an animal RA model. Taken together, fractalkine and its receptor may be a new target molecule for treatment of RA. |
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