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作 者:黄树林[1] 周继斌[1] 陈维春[1] 林月霞[1] 邓涛[1] 罗利琼[1] 肖兰凤[1] 杨红[1]
机构地区:[1]广东药学院分子生物学研究室,广州510224
出 处:《中国免疫学杂志》2001年第5期245-248,共4页Chinese Journal of Immunology
基 金:国家自然科学基金 !批准号 :39770 6 98;广东省自然科学基金 !批准号 :380 838;广东省 :"五个一"基金 !粤卫科 1996 [2 0 ]联合
摘 要:目的 :研究特异识别肝癌细胞株肿瘤相关抗原的TCRVβ基因亚家族的优势取用及对肝癌细胞凋亡的诱导。 方法 :流式细胞术检测淋巴细胞表型 ,RT PCR和Southern印迹分析TCRVβ基因亚家族表达水平 ,Westernblot检测PTK含量。透射电镜观察凋亡细胞超微结构。结果 :McAb共刺激T细胞与肝癌细胞混合培养后 ,T细胞表面CD3和CD8分子表达量明显升高 ,而CD4无明显变化。TCRVβ7选择性扩增 ,表达水平由 5 %升高至 13 %~ 2 5 % ,且在第 4天达到高峰。同时相应的PTK信号传导途径被激活 ,其含量由 11%升至 5 8% ,亦在第 4,5天达到高峰。以抗CD3+CD2 8,抗CD2 8+CD80 ,抗CD2 +CD5 8共刺激的淋巴细胞均在体外诱导了肝癌细胞的凋亡。结论 :TCRVβ7为特异的肿瘤抗原识别受体 ,TCR CD4复合物与抗原结合后激活PTK信号传导途径 。Objective:To study the expression of TCRVβ subfamily which specially recognize the hepatoma cell antigen and the apoptosis of hepatoma cell induced by McAb costimulated PBLs.Methods:The change of the phenotype of PBLs was studied by flow cell cytometry and the level of the expression of TCRVβ was studied by RT-PCR and Southern blot,the PTK by western blot.The hypermicroscopic ultrastructure was observed through transmission electron microscope.Results:The level of CD3 and CD8 of PBLs was significantly increased after acted with hepatoma cells,while there was no change in CD4.The expression of TCRVβ7 of PBLs was dramaticly increased and peaked at 4 days.PTK increased correspondently,to 58% compared with 11% in control.Besides anti-CD3 McAb induced lymphocyte apoptosis,the mediated apoptosis of hepatoma cells was found in the other three groups.Conclusion:TCRVβ7 was the tumor antigen specific T cell receptor,and it activate the PTK signal pathway.The McAb activated lymphocytes initiated apoptosis in hepatoma cells.
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