肝癌细胞通过Fas/FasL途径触发T淋巴细胞的凋亡

Hepatocellular carcinoma cells induced apoptosis of T lymphocytes through Fas/FasL system

目的 :研究肝癌细胞表面 Fas/ Fas L系统的变化及对其逃避机体免疫监控的影响。 方法 :采用流式细胞术和RT- PCR检测肝癌细胞株 Hep G2、Hep3B和 PL C/ PRF/ 5 Fas和 Fas L的表达 ;观察化疗药物争光霉素诱导肝癌细胞 Fas L表达及 Fas L表达上调后的肝癌细胞触发淋巴细胞株 Jurkat细胞凋亡的作用。结果 :Hep G2、Hep3B和 PL C/ PRF/ 5肝癌细胞株Fas表达均阴性 ;Hep G2 Fas L m RNA的表达为阴性 ,而 Hep3B和 PL C/ PRF/ 5 Fas L m RNA的表达均阳性。经争光霉素(0 .6 mg/ m l)诱导后 ,上述肝癌细胞 Fas的表达无明显变化 ,而其 Fas L的表达却增加 ,与 Jurkat细胞混合孵育则触发后者发生显著性凋亡。结论 :肝癌细胞可能一方面降低或不表达 Fas而对 Fas介导的凋亡耐受 ,另一方面又增强自身 Fas L的表达以诱发与之接触的 T淋巴细胞凋亡 ,在完成免疫逃避的同时 ,可对周围的

Objective: To investigate the mechanism of tumor escape through the Fas/FasL system in hepatocellular carcinoma cells (HCC). Methods: Three HCCs were investigated for their expression of Fas and FasL by flow cytometry and RT PCR. HCCs were treated by serial concentration of cytostatic drug bleomycins and Jurkat T cells apoptosis was assessed by co culturing with the treated HCCs. Results: Fas expression of above 3 HCCs was negative, and Jurkat T cells were killed by these 3 HCCs on which FasL induced after treated with bleomycin 0.6 mg/ml. Conclusion: These results suggest that a counterattack model of immune escape of HCCs may exist through Fas/FasL system, whereby cancer cells resist Fas mediated apoptosis by loss of the Fas and kill lymphocyte through the aberrant expression of functional FasL. [