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创伤后巨噬细胞抑制T细胞功能的分子机制研究 |
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梁华平 王正国 朱佩芳 罗艳 耿波 徐祥
摘 要 目的：研究创伤后巨噬细胞抑制T细胞功能的分子机制。方法：将创伤小鼠的巨噬细胞，加入至正常小鼠T细胞培养系统中，测定T细胞功能及细胞内信使分子。结果：创伤后巨噬细胞在体外可明显抑制经ConA刺激的正常T淋巴细胞转化、白介素2(IL-2)的生成、IL-2受体α(IL-2α)的表达以及IL-2 mRNA、IL-2Rα mRNA水平，可升高正常活化T细胞内cAMP含量，降低cGMP含量、游离钙(［Ca2+］i)浓度及蛋白激酶C(PKC)活性。去除创伤小鼠脾细胞中的巨噬细胞，可不同程度地逆转T细胞功能的受抑状态，并降低cAMP含量，增加cGMP含量、［Ca2+］i浓度及PKC活性。结论：创伤后巨噬细胞可通过改变活化T细胞内信使分子水平，进而抑制T细胞功能。
关键词 创伤 巨噬细胞 T淋巴细胞
中国图书分类号 R 640.3
Molecular mechanism of suppressive effect of macrophages from traumatized mice on T cell functions
LIANG Hua-Ping, WANG Zheng-Guo, ZHU Pei-Fang et al. Research Institute of Surgery, Daping Hospital, Third Military Medical University, Chongqing 400042
Abstract Objective:To study molecular mechanism of suppressive effect of macrophages from traumatized mice on T cell functions. Methods:Macrophages from traumatized mice were added into the culture system of normal T cells and then T cell functions and intracellular messenger molecules were determined. Results:Macrophages from traumatized mice could obviously suppress transformation of normal T lymphocyte stimulated with ConA, interleukin 2(IL-2) production, IL-2 receptor α(IL-2Rα) expression ,IL-2 mRNA and IL-2R mRNA levels, and could elevate cAMP contents of activated normal T cells while decreasing cGMP contents, free calcium(［Ca2+］i) concentration and protein kinase C(PKC) activity. Removal of macrophages from splenocytes of traumatized mice could at various degree reverse the suppression of T cell functions, decrease cAMP contents while increasing cGMP contents, ［Ca2+］i concentration and PKC activity. Conclusions:Macrophages from traumatized mice may suppress T cell functions via altering messenger molecule levels in activated T cells.
Key words Trauma Macrophage T lymphocyte
严重创伤后巨噬细胞免疫抑制活性增强是导致T细胞功能受抑的重要原因之一。以往研究证实，创伤后巨噬细胞可通过分泌大量的PGE2及直接的细胞接触方式发挥其对T淋巴细胞功能的抑制效应［1，2］。但对其抑制T细胞功能的分子机制尚不清楚，本研究[1] [2] 下一页
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