【摘要】 目的　探讨肾癌Fas表达异常与免疫逃避的关系及其调控。方法　采用免疫组织化学技术检测 44例肾癌组织的Fas、Ki 67表达。以细胞因子诱导肾癌细胞株 786 0、GRC 1Fas表达 ,以Fas单克隆抗体 (FasAb)诱导其凋亡。结果　 (1)肾癌组织Fas表达阳性率 (2 2 .8% )显著低于正常肾组织 (5 3 .8% ,P <0 .0 1)。肾癌Ki 67表达阳性率 3 2 .8%。肾癌Fas表达与Ki 67表达呈显著负相关 (r =-0 .62 ,P <0 .0 5 )。临床分期Ⅲ期、Ⅳ期患者Fas表达显著低于Ⅰ期 (P <0 .0 1)。(2 )IFN α、IFN γ均能显著提高肾癌细胞株 786 0、GRC 1的Fas表达 ,并促进FasAb介导的凋亡。IL 2、TNF α无此作用。TNF α能增强IFN α诱导的Fas表达 ,并增强FasAb介导的凋亡。结论　肾癌通过下调Fas表达实现免疫逃避。IFN γ、IFN α可通过上调肾癌细胞Fas表达促进Fas介导的凋亡。更多还原

【Abstract】 Objective To investigate the mechanism of immune escape in renal cell carcinoma (RCC).Methods The Fas and Ki-67 expression was detected by immunohistochemical technique in 44 cases of RCC.Cytokines were used to induce the expression of the renal carcinoma cell lines 786-0 and GRC-1.Combined treatment of 786-0 and GRC-1 with cytokines and Anti-Fas monoclonal antibody (FasAb) was performed to induce apoptosis.Results (1) Fas expression rate in RCC was lower than that in the controlled normal kidney tissues (P< 0.01).Ki-67 expression rate in RCC was 32.8%.The expression of Fas and Ki-67 had a negative correlation (r= -0.62, P< 0.05).The Fas expression of stage Ⅰ was significantly higher than that of stage Ⅲ and Ⅳ.(2) IFN-γ and IFN-α could up-regulate the Fas expression and subsequently augmente the Fas-mediated apoptosis in 786-0 and GRC-1 cells,but IL-2 and TNF-α had no same effects.The combination of TNF-α and IFN-α synergistically enhanced the Fas expression and FasAb-mediated apoptosis of 786-0 and GRC-1 cells.Conclusion Down-regulation of Fas expression is one of mechanisms for RCC cells to escape immune attack.by enhancement of Fas expression,IFN-γ and IFN-α augmenting the Fas-mediated apoptosis of RCC cells.更多还原