摘要
为研究细胞因子对肾癌细胞株 786 0Fas表达以及FasAb介导凋亡的影响 ,单独或联合应用IFN γ ,IFN α ,IL 2 ,TNF α刺激 786 0细胞株 ,并以Fas单克隆抗体 (FasAb )诱导其凋亡。结果发现 ,IFN α、IFN γ均能显著上调 786 0细胞的Fas表达 (P <0 0 1,P <0 0 1)并促进FasAb诱导的凋亡 (P <0 0 1,P <0 0 1) ;IL 2、TNF α对 786 0的Fas表达及FasAb诱导的凋亡均无影响 ;IL 2不能增强IFN α、IFN γ诱导的Fas表达 ,亦不能促进凋亡。TNF α能增强IFN α诱导的Fas表达并促进凋亡 ,但不影响IFN γ诱导的Fas表达及其凋亡。结果表明IFN γ、IFN α可增强肾癌细胞株 786 0的Fas表达 ,并促进FasAb介导的凋亡。
To study the effects of cytokines on the Fas expression on renal cell carcinoma cell line 786 0 and the induction of Fas mediated apoptosis,the 786 0 cell line was stimulated with IFN α,IFN γ,IL 2 and TNF α individually or in combinations,and the apoptosis was induced by anti Fas monoclonal antibody(FasAb). It was found that IFN α and IFN γ both synergistically up regulated the Fas expressions of the 786 0 cells,and promoted the Fas mediated apoptosis,but neither IL 2 nor TNF α showed the same effect The combination uses of TNF α and IFN α synergistically enhanced the Fas expressions and the induction of Fas mediated apoptosis of the 786 0 cells,but the combinations of TNF α and IFN γ did not show any synergistic effect These results indicate that IFN γ and IFN α could augment the Fas mediated apoptosis of the 786 0 cells by enhancement of the Fas expression,but the sensitivity to the induction of Fas mediated apoptosis seems to be not completely dependent on the levels of cell surface Fas
出处
《上海免疫学杂志》
CSCD
北大核心
2002年第3期189-190,148,共3页
Shanghai Journal of Immunology
基金
江苏省自然科学基金资助项目 (BS983 19)
关键词
肾癌细胞
细胞因子
FAS
凋亡
renal cell carcinoma cell
Fas
cytokine
apoptosis