目的：通过ｂｃｌ２阻断Ｆａｓ介导的细胞凋亡了解ｂｃｌ２基因在淋巴瘤癌变过程中逃避机体免疫监控的作用机制。方法：应用基因重组技术重组ｐＬＸＳＮｂｃｌ２，采用电穿孔法将其与空载体分别转染包装细胞系ＰＡ３１７，将阳性克隆病毒上清感染人Ｔ淋巴瘤细胞株Ｊｕｒｋａｔ，用Ｇ４１８筛选，其阳性克隆进行免疫组化检测，应用抗Ｆａｓ抗体诱导细胞凋亡来模拟细胞毒Ｔ细胞的杀伤机制，观察ｂｃｌ２在淋巴瘤逃避免疫机制中的作用。结果：转染人ｂｃｌ２基因的Ｊｕｒｋａｔ（Ｊｕｒｋａｔｂｃｌ２）细胞较对照Ｊｕｒｋａｔ及转染空载体Ｊｕｒｋａｔ（Ｊｕｒｋａｔｎｅｏ）细胞，ｂｃｌ２表达量明显增加，而Ｆａｓ基因表达量无明显变化。其Ｊｕｒｋａｔｂｃｌ２能明显耐受抗Ｆａｓ抗体诱导的细胞凋亡。结论：人ｂｃｌ２基因在淋巴瘤中过量表达，能部分阻断抗Ｆａｓ抗体诱导的细胞凋亡，ｂｃｌ２基因过量表达可能是淋巴瘤癌变过程中逃脱机体免疫监控的机制之一。 OBJECTIVE: To investigate the mechanism of bcl-2 gene escape from immune surveillance in the process of carcinogenesis of lymphoma through bcl-2 blocking Fas-mediated apoptosis. Methods: Recombinant pLXSN-bcl-2 was recombined by gene recombination technique and transfected into PA317 packaging cell line by electroporation. The positive clones were infected with Jurkat cell line of human T lymphoma cells and screened by G418 Positive clones were detected by immunohistochemistry, anti-Fas antibody-induced apoptosis to mimic cytotoxic T-cell killing mechanism observed bcl 2 in lymphoma escape immune function. Results: Jurkat (Jurkatbcl2) cells transfected with human bcl2 gene showed significantly increased expression of bcl2 compared with Jurkat (Jurkatneo) cells transfected with empty vector, while the expression of Fas gene was not significant Variety. The Jurkat bcl 2 can significantly tolerate anti-Fas antibody-induced apoptosis. Conclusion: The overexpression of human bcl2 gene in lymphoma can partly block the apoptosis induced by anti-Fas antibody. The overexpression of bcl2 may be one of the mechanisms of escaped immune surveillance during the carcinogenesis of lymphoma.