幽门螺杆菌致T细胞凋亡：Fas/FasL介导的T细胞无反应性

目的 评价幽门杆菌（Hp）致T细胞死亡的方式和机制，探讨这种作用与Hp感染致宿主产生免疫耐受的关系。方法 应用AnnexinV染色流式细胞术检测Hp致T细胞死亡的方式；应用细胞毒实验（JAM技术）和FasIgG抗体、caspase8抑制剂组断实验评价T细胞凋亡与Fas/FasL作用的关系，并通过流式细胞术直接检测Hp对T细胞FasL表达的上调作用及其与T细胞产生凋亡的时效关系。结果 AnnexinV染色和JAM技术证实H致T慢以凋亡方式进行的。这种细胞凋亡能被抗Fas抗体和caspase8抑制剂阻断，因而是Fas依赖，TH2细胞较TH1样T细胞对这种作用更敏感。由于Hp能直接上调T细胞的FasL且其发生时间与凋亡出现时间吻合，证实Hp是通过凋节T细胞之间Fas/FasL相互作用而致其凋亡的。Hp能通过调节Fas/FasL作用而负调节T细胞的生长，这可能是Hp感染致宿主发生T细胞耐受的机制之一。

cell anergy during Helicobacter pylori infection stems from the apoptosis mediated by Fas/FasL interaction

Objective Helicobacter pylori (H. pylori ) was capable of inhibiting T cell growth in vitro and this may explain the anergy of T cell to the infection in vivo . To elucidate this mechanism, T cell apoptosis was studied when exposed to H. pylori . Methods T cell apoptosis was identified by flow cytometry to detect the binding to Annexin V after the incubation with H. pylori . A co culture cytotoxicity assay (JAM) was used to evaluate the mechanism of T cell apoptosis. Fas ligand (FasL) expression on T cells was also detected by flowcytometry. Results Cell apoptosis in T cell lines (Jurkat and Cem C7) initiated after exposure to H. pylori as proven by Annexin V staining assay. The susceptibility of T H2 cell line Cem C7 to H. pylori was higher than that of non T H2 cell line. T cell apoptosis caused by H. pylori could be blocked by anti Fas blocking antibody and caspase 8 inhibitor. It suggested that the T cell apoptosis was mediated by Fas/FasL system. Direct detection of FasL expression indicated that H. pylori was capable of up regulating FasL expression on T cell and this happened coincidentally with the arising potential of T cell apoptosis. Conclusion Fas/FasL mediated apoptotic suicide or patricide of T cells, especially T H2 cells induced by H. pylori may explain the T cell anergy during the infection.