中文摘要：

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-7和IL-12 p40 mRNA水平明显低于野生型对照小鼠，3h2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-7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。

英文摘要：

Objective To explore the role of lymphocyte function-associated antigen-1 （ LFA-1 ） in the development of rheumatoid arthritis.Melhods Establish mouse model of rheumatoid arthritis by induction with collagen type H . 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 type Ⅱ , the IFN-γ and IL-12 p40 mRNA levels in draining lymph nodes and joints of mice with knock-out of LFA-I gene were significandy 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.