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McAb共刺激PBLs膜表面分子表达与肝癌细胞凋亡的相关性
引用本文:明利华,陈维春,林月霞,黄树林,符生苗,邓立群. McAb共刺激PBLs膜表面分子表达与肝癌细胞凋亡的相关性[J]. 中国免疫学杂志, 2001, 17(4): 195-197
作者姓名:明利华  陈维春  林月霞  黄树林  符生苗  邓立群
作者单位:1. 中国医学院学院肿瘤研究所博士生,
2. 广东药学院分子生物学研究室,
3. 海南省人民医院
摘    要:目的研究McAb共刺激PBLs前后的表型变化及与肝癌细胞凋亡的相关性。方法采用流式细胞仪分析PBLs被刺激前后的表型,用电镜超微结构和DNA梯子电泳观察肝癌细胞凋亡。结果CD3、CD4分子表达高于刺激前约10%,肝癌细胞出现凋亡,细胞核固缩、边聚、裂解。同时也出现典型的DNA梯子。而肝癌患者用共刺激PBLs后,CD3和CD8增高(P<0.05)。结论共刺激使共刺激信号分子增加,抗原呈递能力增强,也使细胞因子分泌增加,这些因素促使肝癌细胞凋亡,而肿瘤患者T细胞增加时向CD8

关 键 词:单抗共刺激 肝癌细胞 细胞凋亡 McAb PBLS膜表达分子
文章编号:1000-484X(2001)04-0195-03

Correlation of McAbcostimulation PBLs membrane surface molecular expression and hepatoma cell apoptosis
MING Li Hua,CHEN Wei Chun,LIN Yue Xia et al. Correlation of McAbcostimulation PBLs membrane surface molecular expression and hepatoma cell apoptosis[J]. Chinese Journal of Immunology, 2001, 17(4): 195-197
Authors:MING Li Hua  CHEN Wei Chun  LIN Yue Xia et al
Affiliation:MING Li Hua,CHEN Wei Chun,LIN Yue Xia et al.Department of Molecular Biology,Guangdong Pharmacy College,Guangzhou 510224
Abstract:objective:To study phenotype changes in PBLs costimulated by McAb and correlation of phenotype changes and apoptosias in hepatoma cell.Methods:Cell phenotype changes in PBLs were analyzed of flow cytometry.By mean of hypermicroscopic structure and DNA ladder electrophoresis,hepatoma cell apoptosis was studied.Results:Expression of CD3、CD4 in stimulated PBLs was about 10 percent more than those eithout stimulation Nucleus pyknotic、border gathering and collapse were found in hepatoma cell, which showed typical apoptosis.DNA ladder appeared in electrophoresis of hepatoma DNA.CD3 and CD8 increased in tumor patients PBLs being co-stimulated(P<0.05).Conclusion:Co-stimulatng signal molecular increased,presenting antigen enhanced and cytokine secreted more by co-stumulating. Hepatoma cell apoptosis was bringed by these factors. T cell of tumor patientiated to CD8+ . Correlation of membrane molecular expression and apoptosis was showed by the results.
Keywords:McAb co stimulation Membrane molecular Hepatoma cell Apoptosis
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