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  

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

作　　者：王轶楠[1] 常非[2] 陈方方[1] 马迪[1] 霍德胜[1] 柳忠辉[1] 

机构地区：[1]吉林大学基础医学院免疫学教研室吉林省神经免疫重点实验室,长春130021 [2]吉林大学中日联谊医院骨科,长春130031

出　　处：《中国生物制品学杂志》2007年第12期877-879,共3页Chinese Journal of Biologicals

基　　金：国家自然科学基金(30671953);吉林省科技厅项目(20040707-6).

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-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。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.

关 键 词：淋巴细胞功能相关抗原1(LFA-1) 类风湿性关节炎 引流淋巴结 关节 T细胞活性 

分 类 号：Q789[生物学—分子生物学]