肝癌细胞通过Fas/FasL途径触发T淋巴细胞的凋亡

目的：研究肝癌细胞表面Fas/FasL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HepG2、Hep3B和PLC/PRF/5Fas和FasL的表达；观察化疗药物争光霉素诱导肝癌细胞FasL表达及FasL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：HepG2、Hep3B和PLC/PRF/5肝癌细胞株Fas表达均阴性；HepG2 FasL mRNA的表达为阴性，而Hep3B 和PLC/PRF/5FasL mRNA的表达均阳性。经争光霉素（0.6mg/ml）诱导后，上述肝癌细胞Fas的表达无明显变化，而其FasL的表达却增加，与Jurkat细胞混合孵育则触发后发生显性调亡。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FasL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T细胞实施反攻击。

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

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.