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目的 探讨肾癌免疫逃避机制。方法 采用免疫组化技术检测 44例肾癌组织的Fas、FasL、Ki6 7表达以及肿瘤周围浸润淋巴细胞 (TIL)的凋亡。体外实验应用细胞因子IL2、IFNα诱导肾癌细胞株 786 0Fas表达 ,以Fas单克隆抗体 (FasAb)诱导其凋亡。应用 786 0与JurkatT淋巴细胞共培养的方法研究FasL功能。结果 (1)肾癌组织的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) ,肾癌组织的FasL表达阳性率 (4 6 .5 % )显著高于正常肾组织 (2 3.2 % ,P <0 .0 1)。肾癌Ki6 7表达阳性率 32 .8%。肾癌Ki6 7表达与Fas表达呈显著负相关 (r =- 0 .6 2 ,P <0 .0 5 ) ,与FasL表达呈显著正相关 (r=0 .93,P <0 .0 1)。随肾癌临床分期增加 ,Fas表达阳性率减少 (P <0 .0 1) ,FasL表达阳性率增加 (P <0 .0 1)。 (2 )肾癌组织的TIL凋亡率 (33.9% )显著高于正常肾组织的TIL凋亡率 (3.5 % ,P <0 .0 1)。肾癌FasL表达率与TIL凋亡率呈显著正相关 (r =0 .96 ,P <0 .0 1)。 (3) 786 0细胞Fas表达率为 13.7% ,FasAb诱导其凋亡率为 9.6 % ,IFNα能显著提高 786 0的Fas表达 (30 .2 % ,P <0 .0 1) ,并促进FasAb诱导的凋亡 (2 6 .8% ,P <0 .0 1) ,IL2无此作用。 (4 ) 786 0FasL表达率 18.6 % ;Jurkat细胞与 786 0细胞
Objective To investigate the immune escape mechanism of renal cell carcinoma. Methods The expressions of Fas, FasL and Ki6 7 in 44 cases of renal cell carcinoma and the infiltration of lymphocytes (TIL) around the tumor were detected by immunohistochemistry. The cytokines IL2 and IFNα were used to induce 786 O Fas expression in renal carcinoma cell line in vitro, and the apoptosis was induced by Fas monoclonal antibody (FasAb). FasL function was studied using 786 0 co-culture with Jurkat T lymphocytes. Results (1) The positive rate of Fas expression in renal cell carcinoma (22.8%) was significantly lower than that in normal renal tissue (53.8%, P <0.01). 5%) was significantly higher than that of normal renal tissue (23.2%, P <0.01). The positive rate of Ki6 7 in renal cell carcinoma was 32.8%. The expression of Ki6 7 in renal cell carcinoma was negatively correlated with the expression of Fas (r = - 0.62, P <0.05), which was positively correlated with the expression of FasL (r = 0.93, P <0.01) . With the increase of clinical stage of renal cell carcinoma, the positive rate of Fas expression was decreased (P <0.01), and the positive rate of FasL expression was increased (P <0.01). (2) The apoptosis rate of TIL in renal cell carcinoma (33.9%) was significantly higher than that in normal renal tissue (3.5%, P <0.01). There was a significant positive correlation between FasL expression rate and TIL apoptosis rate (r = 0.96, P <0.01). (3) The Fas expression rate of 786 0 cells was 13.7%, FasA induced apoptosis rate was 9.6%, IFNα significantly increased 786 0 Fas expression (30.2%, P <0.01), and promoted FasAb induction (26.8%, P <0.01), IL2 had no such effect. (4) 786 0FasL expression rate of 18.6%; Jurkat cells and 786 0 cells