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目的 查明趋化因子C C亚族受体 5 (CCR5 )及其配体在外周血、关节滑膜和滑液的表达及分布 ,探讨Th1细胞选择性聚集于类风湿关节炎 (RA)患者关节中的机制。方法 采用两色和三色免疫荧光标记、流式细胞术及激光扫描共聚焦显微技术 ,对 15例RA患者外周血、关节液及滑膜中Th细胞亚群 ,以及趋化因子受体CCR5和CXCR3的表达细胞 ,和C C亚族趋化因子巨噬细胞炎性蛋白 (MIP) 1β的产生细胞 ,进行了测定和分析比较。 结果 (1)RA患者关节滑液细胞内细胞因子分泌模式明显向Th1偏移 ,Th1样细胞在关节内占优势。 (2 )RA患者滑液中T细胞受体CCR5的表达率为5 2 %± 8% ,CXCR3的表达率为 6 1%± 12 % ,与自身及正常人 (外周血单个核细胞 )比较明显升高 (P <0 .0 1)。 (3)RA患者滑膜组织中大量浸润的T细胞 (尤其是CD4 + 细胞 )、单核 /巨噬细胞 (Mo/Mac)、B细胞多表达CCR5的配体MIP 1β。 结论 RA患者的关节内 ,T细胞、B细胞、Mo Mac产生MIP 1β、RANTERS等趋化因子 ,能趋化表达CCR5、CXCR3的Th1细胞选择性进入关节组织 ,导致Th1/Th2细胞失衡
Objective To investigate the expression and distribution of chemokine CC subunit 5 (CCR5) and its ligand in peripheral blood, synovial fluid and synovial fluid, and to explore the role of Th1 cells in the selective aggregation of the joints of patients with rheumatoid arthritis (RA) In the mechanism. Methods Two-color and three-color immunofluorescence staining, flow cytometry and laser scanning confocal microscopy were used to detect the Th cell subsets in peripheral blood, synovial fluid and synovium in 15 patients with RA, as well as the chemokine receptor CCR5 And CXCR3-expressing cells, and CC subunit chemokine macrophage inflammatory protein (MIP) 1β-producing cells, were measured and compared. Results (1) The pattern of intracellular cytokine secretion in synovial fluid of RA patients was significantly shifted to Th1, and Th1-like cells were dominant in the joints. (2) The expression rate of CCR5 in the synovial fluid of rheumatoid arthritis patients was 52% ± 8% and CXCR3 was 61% ± 12% in RA patients, which was significantly higher than those in peripheral blood mononuclear cells Increased (P <0. 01). (3) Large numbers of infiltrating T cells (especially CD4 + cells) and monocytes / macrophages (Mo / Mac) in synovial tissue of RA patients, and B cells overexpressing ligand MIP 1β of CCR5. CONCLUSIONS: MIP 1β, RANTERS and other chemokines are produced in joints, T cells, B cells and Mo Macs of RA patients, which can selectively enter Th1 cells expressing CCR5 and CXCR3 into joint tissues and result in imbalance of Th1 / Th2 cells