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目的:探讨心肌梗死后介导自身免疫应答和细胞因子分泌的细胞类型。方法:体外分离同源大鼠T细胞和树突状细胞,与大鼠心肌肌球蛋白共培养,使T细胞活化,然后将活化的、未活化的T细胞分别过继转输给同源大鼠(转输组、对照组),观察3d、1周和4周后心肌的病理改变,分别采用免疫组织化学和RT-PCR的方法检测各时间点白细胞介素-6(IL-6)蛋白和mRNA的表达。结果:转输组大鼠心肌有不同程度地炎性细胞浸润,主要为淋巴细胞,偶见心肌水肿、变性及坏死,炎性细胞浸润以1周最明显,呈弥漫性;对照组大鼠心肌未见类似病理改变。转输组IL-6mRNA和蛋白表达在转输后3d开始升高,1周末达到高峰,4周末开始下降,1周末和4周末心肌组织的IL-6mRNA和蛋白表达均明显高于对照组(P<0·01)。结论:T细胞介导心肌自身免疫性炎症的发生,同时也促使心肌细胞致炎因子IL-6的表达,共同导致急性心肌梗死后心肌细胞的损伤。
Objective: To investigate the cell types that mediate the autoimmune response and cytokine secretion after myocardial infarction. Methods: T cells and dendritic cells of homologous rats were isolated in vitro and co-cultured with rat cardiac myosin to activate T cells. Subsequently, activated and non-activated T cells were adoptively transferred to homologous rats (Transfusion group and control group). The pathological changes of myocardium were observed after 3d, 1 week and 4 weeks respectively. The expressions of IL-6 and IL-6 at each time point were detected by immunohistochemistry and RT-PCR respectively mRNA expression. Results: The myocardial cells in the transfused group had infiltration of inflammatory cells in varying degrees, mainly lymphocytes, and occasionally myocardial edema, degeneration and necrosis. Inflammatory cell infiltration was the most obvious and diffuse in 1 week. In the control group, No similar pathological changes. The level of IL-6mRNA and protein in the transfused group began to increase 3 days after transfusion, peaked at 1 week, then decreased at the end of 4 weeks, IL-6mRNA and protein expression in myocardial tissue at 1 week and 4 week were significantly higher than those in control group <0 · 01). CONCLUSION: T cells mediate the occurrence of myocardial autoimmune inflammation and promote the expression of IL-6, a factor that contributes to the cardiomyocyte injury after acute myocardial infarction.