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逄曙光, 赵家军, 刘子栋, 高聆, 王波. CD8+T细胞在糖尿病发病中作用[J]. 中国公共卫生, 2007, 23(7): 840-842. DOI: 10.11847/zgggws2007-23-07-36
引用本文: 逄曙光, 赵家军, 刘子栋, 高聆, 王波. CD8+T细胞在糖尿病发病中作用[J]. 中国公共卫生, 2007, 23(7): 840-842. DOI: 10.11847/zgggws2007-23-07-36
PANG Shu-guang, ZHAO Jia-jun, LIU Zi-dong, . Study on role of CD8+Tcells in development of diabetes[J]. Chinese Journal of Public Health, 2007, 23(7): 840-842. DOI: 10.11847/zgggws2007-23-07-36
Citation: PANG Shu-guang, ZHAO Jia-jun, LIU Zi-dong, . Study on role of CD8+Tcells in development of diabetes[J]. Chinese Journal of Public Health, 2007, 23(7): 840-842. DOI: 10.11847/zgggws2007-23-07-36

CD8+T细胞在糖尿病发病中作用

Study on role of CD8+Tcells in development of diabetes

  • 摘要: 目的 探讨CD8+T细胞在糖尿病发病中的作用。方法 利用非肥胖糖尿病(NOD)背景的转基因小鼠,将CD4+T细胞和CD8+T细胞过继转移到有T细胞缺陷的NOD小鼠(即NOD.scid小鼠),同时转移到特异性地在β细胞上表达共刺激分子CD80的有T细胞缺陷的NOD小鼠(即NOD.scid.Rip.B7小鼠),观察两组受鼠胰岛炎和糖尿病的发病情况,并分析其差异。结果 转移CD4+T细胞时,糖尿病发病率在NOD.scid受鼠和NOD.scid.Rip.B7受鼠组的差异无统计学意义(P>0.05),转移CD8+T细胞时,NOD.scid受鼠糖尿病发病率低于NOD.scid.Rip.B7组受鼠,差异有统计学意义(P<0.001)。结论 CD8+T亚群启动了胰岛的淋巴细胞浸润,CD8+T细胞是通过与胰岛β细胞直接作用启动糖尿病的发生。

     

    Abstract: Objective To investigate the role of CD8+T cells in the pathogenesis of diabetes.Methods CD4+T cells and CD8+T cells were respectively transferred from genetically-engineered non-obese diabetic(NOD)mice and NOD background mice to T cell-deficient NOD mice(i.e.NOD.scid mice)and T cell-deficient NOD mice with co-stimulating molecules CD80 expressed specific on islets B cells(i.e.NOD.scid.Rip.B7 mice).Insulitis and diabetes were monitored in the two recipients and the difference between the two recipients was analyzed.Results There was no significant difference in incidence of diabetes between recipients of NOD.scid mice and NOD.scid.R ip.B7 mice when CD4+T cells were transfer red (P>0.05).However,when CD8+T cells were transfer red,the incidence of diabetes in NOD.scid recipients was significantly lower than that of in NOD.scid.Rip.B7 recipients(P<0.001).Conclusion CD8+T cells triggers the infiltration of the pancreatic islets,CD8+T cells initiate diabetes by direct interaction with islet beta cells.

     

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