摘要
目的 :研究细胞因子对肾癌株Fas、FasL表达的影响及其意义。方法 :单独或联合应用IFNγ ,IFNα ,IL 2 ,TNFα刺激肾癌株 786 0、GRC 1细胞并检测Fas、FasL表达 ,以Fas单克隆抗体 (FasAb)诱导其凋亡 ,以JurkatT细胞共培养试验检测其FasL功能。结果 :1 IFNγ、IFNα均能显著上调 786 0、GRC 1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)。 2 TNFα、IFNα能分别上调 786 0、GRC 1细胞的FasL表达。IFNγ能显著上调 786 0、GRC 1细胞的FasL表达(P<0 0 1,P <0 0 1) ,并促进JurkatT细胞凋亡 (P <0 0 1,P <0 0 1)。结论 :IFNγ、IFNα可增强肾癌细胞株的Fas表达 ,并促进FasAb介导的凋亡。但其亦能上调肾癌细胞FasL表达并增强其对淋巴细胞的攻击作用。
Objective:To investigate the role of cytokines in modulating expression of Fas and FasL in renal cell carcinoma cells(RCCs) and its implication.Methods:Combination treatment of 786 0 and GRC 1 cells with cytokines including IFNγ?IFNα,IL 2,TNFα and anti Fas monoclonal antibody (FasAb) to induc apoptosis.FasL function was assessed by coculture assays in vitro using renal cancer cells 786 0 or GRC 1 and Fas sensitive Jurkate T cells.Results:1.Either IFNγ or IFNα could up regulate the Fas expression and subsequently augment the Fas mediated apoptosis in 786 0 and GRC 1 cells.2.IFNγ and IFNα could up regulate the FasL expression in 780 0 and GRC 1 cells.And subsequently augmente the apoptosis of Jurkat T cells cocultured with 786 0 and GRC 1 cells.IFNα had the same effects on 786 0 cells.IFNα had the same effects on GRC 1 cells.Conclusion:IFNγ and IFNα could agument the Fas mediated apoptosis of RCCs by enhancement of Fas expression,but they also up regulate the expression of FasL in RCCs and subsequently augmente the apoptosis of RCCs by enhancment the apoptosis of T lymphocytes by Fas/FasL pathway.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
2002年第11期766-768,共3页
Chinese Journal of Immunology
基金
江苏省科学基金资助 (BS983 19)
