miR-150缺失增强小鼠NKT细胞IFN-γ产生并促进小鼠Ⅰ型糖尿病的发生

摘要

Objective:To explore the role of miR-150 in the function of NKT cell and the occurrence of type Ⅰ diabetes in mice.Methods:miR-150 knock out mice were used and the quantity of peripheral NKT cells were detected by Flow cytometry.Cytokine production was detected by intracellular staining and ELISA.STZ was used to induce type Ⅰ diabetes of wild type and miR-150 knock out mice,and the occurrence of diabetes was assessed after o-Galcer treatment.Results:miR-150 deletion resulted in the increased IFN-γ production of NKT cells,while did not affect the number of peripheral NKT cells.In addition,the occurrence of type Ⅰ diabetes was accelerated in α-Galcer treated miR-150 knock out mice compared with wild type mice.Conclusion:miR-150 deletion increased IFN-γ production of NKT cells,and activated miR-150 knock out NKT cell accelerated the occurrence of diabetes in mice.%目的:探讨miR-150在小鼠NKT细胞免疫功能中的作用及对小鼠Ⅰ型糖尿病发生的影响.方法:采用miR-150基因敲除小鼠;流式细胞术检测小鼠外周免疫器官NKT细胞数量变化;细胞内染色和ELISA检测NKT细胞因子的表达和分泌;采用STZ处理建立Ⅰ型糖尿病小鼠模型,体内注射α-Galcer活化NKT细胞,观察miR-150敲除对小鼠糖尿病发生的影响.结果:miR-150基因缺失不影响小鼠外周NKT细胞的数量,但导致NKT细胞IFN-γ产生显著增加;采用STZ处理小鼠并同时给予α-Galcer活化NKT细胞,发现miR-150敲除加速小鼠糖尿病的发生.结论:miR-150基因敲除促进小鼠NKT细胞IFN-γ的产生,活化miR-150敲除NKT细胞加速小鼠Ⅰ型糖尿病的发生.