热休克蛋白60对小鼠树突状细胞功能影响体外研究  

Effect of heat shock protein 60 on murine dendritic cell function in vitro

作　　者：吴伟[1] 李大主[1] 周游[1] 曾秋棠[1] 

机构地区：[1]华中科技大学同济医学院协和医院心内科,武汉430022

出　　处：《中国免疫学杂志》2007年第3期208-211,共4页Chinese Journal of Immunology

摘　　要：目的探讨动脉粥样硬化中重要炎性物质——热休克蛋白60(HSP60)体外对小鼠树突状细胞(mDC)功能影响。方法小鼠骨髓提取DC,体外培养成熟后与两种浓度mHSP60孵育,动态观察DC突起改变;流式细胞仪检测孵育前后mDC表面标志改变;MLR测定孵育前后mDC刺激功能变化;ELISA法测定MLR上清液中细胞因子浓度。结果孵育后,mDC突起增加明显;CD11c+、CD80及CD86表型显著增加;淋巴细胞刺激功能明显增强;分泌细胞因子IL-12、IFN-γ增加(P<0.01)而IL-4增加不明显(P>0.05),IFN-γ/IL-4比值升高。结论mHSP60体外可以促进mDC功能,作用呈剂量依赖性。Objective ：To investigate the effect of heat shock protein 60 （HSP60）, significant inflammatory factor in atherosclerosis, on the maturation of murine dendritic cells （mDCs） in vitro. Methods ： Myeloid mDCs were extracted in vitro from mouse marrow and incubated to mature with two distinct concentrations of mHSP60. The morphological changes were observed;the variation of phenotype was detected with flow cytometric analysis; the stimulating capacity was determined in allogenic mixed lymphocyte reaction （MLR） ; ELISA was used to analyze the level of cytokines secreted by mDCs and stimulated lymphocyte in the medium of MLR. Restilts： Dendrites of mHSP60-DCs raised obviously. The expression of co-stimulating factor CD11c^＋ , CD86, CD80 was up-regulated. The stimulating capacity of mHSP-DCs in MLR was higher. T lymphocytes co-cuhured with mHSP-DCs in MLR secreted higher levels of pro-inflammation cytokines（ IFN-γ, IL-12） but there were no significant difference of IL-4, the stimulatory action was dose dependent and was evident at higher concentrations. The ratio of IFN-γ/IL-4 was increased. Conclusion ： mHSP60 progressed the maturation of mDC dose-dependently in vitro.

关 键 词：热休克蛋白60 树突状细胞 动脉粥样硬化 表型 细胞因子 

分 类 号：R392.12[医药卫生—免疫学] R541.4[医药卫生—基础医学]