LFA-1基因对胶原诱导小鼠关节炎关节局部引流淋巴结T细胞活性的影响

目的探讨淋巴细胞功能相关抗原1(LFA-1)在类风湿性关节炎形成中的作用。方法采用Ⅱ型胶原诱导小鼠关节炎模型,观察LFA-1基因敲除小鼠引流淋巴结T细胞增殖和细胞因子水平。结果LFA-1基因敲除小鼠在应用Ⅱ型胶原免疫后,引流淋巴结和关节局部Th1型细胞因子IFN-γ和IL-12p40mRNA水平明显低于野生型对照小鼠,Th2型细胞因子IL-4mRNA水平无明显变化。LFA-1基因敲除小鼠引流淋巴结来源的CD4+T细胞在体外受Ⅱ型胶原刺激后,其特异性增殖和细胞因子IFN-γ的产生也明显低于野生型对照小鼠。结论LFA-1基因缺失抑制了辅助性T细胞的活化和向Th1方向的分化,进而抑制关节炎的发生。

Effect of LFA-1 Gene on T Cell Activity in Draining Lymph Nodes and Joints of Mice with Collagen-Induced Rheumatoid Arthrits

Objective To explore the role of lymphocyte function-associated antigen-1(LFA-1)in the development of rheumatoid arthritis.Methods Establish mouse model of rheumatoid arthritis by induction with collagen typeⅡ.Observe the T cell proliferation and cytokine level in draining lymph nodes of mice with knock-out of LFA-1 gene.Results After treatment with collagen typeⅡ,the IFN-γ and IL-12 p40 mRNA levels in draining lymph nodes and joints of mice with knock-out of LFA-1 gene were significantly lower than those of wild mice as control,while the IL-4 mRNA level showed no significant change.After stimulation in vitro with collagen type Ⅱ,the specific proliferation and IFN-γ production of CD4+T cells derived from draining lymph nodes of mice with knock-out of LFA-1 gene were also significantly lower than those of wild mice as control.Conclusion The lack of LFA-1 gene inhibited the activation of helper T cells and its differentiation to Th1 cells,thus suppress the development of arthritis.