首页|活化T细胞膜信号分子表达与结肠癌细胞凋亡的相关性

活化T细胞膜信号分子表达与结肠癌细胞凋亡的相关性

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目的:研究CpG寡脱氧核苷酸(CpG ODN)作用于活化T细胞前、后的膜分子表达及与结肠癌细胞凋亡的相关性.方法:采用流式细胞术检测健康人外周血(PBLs)T细胞被刺激前、后的表型结构和结肠癌细胞凋亡指数变化;采用电镜观察肿瘤细胞超微结构变化.结果:CpG ODN参与刺激作用结肠癌细胞前CD28分子表达略高于刺激前,而CD3分子表达则明显高于刺激前.电镜观察结果显示,效应细胞作用肿瘤细胞48 h时部分肿瘤细胞发生坏死,部分出现凋亡;72 h时肿瘤细胞凋亡明显;而结肠癌患者采用CpG ODN共刺激PBLs后,CD3和CD8增高(P<0.05).结论:CpG ODN共刺激可使T细胞表面信号分子增加,促使细胞因子及其激活的杀伤细胞分泌增加,至结肠癌细胞出现凋亡;肿瘤细胞凋亡与膜分子变化关系密切.
Correlation of activation of T cell signal molecular expression and colon cancer cell apoptosis
AIM: To investigate the correlation of activation of T cell combined with CpG ODN signal molecular expression and colon cancer cell apoptosis. METHODS: Cell phenotype in PBLs were by the flowcytometry. The microchange of the tumor ceils was investigated by electron microscope and the apoptotic index of the colon carcinoma cell was detected by the flow cytometry. RESULTS: Expression of CD28 in stimulated PBLs was a little more than those without stimulation. Cell expression of CD3, CD4 in stimulated PBLs was significantly more than those without stimu lation. Electron microscope verified that tumor cell necrosis occurs after 48 h exposion to costimulate activation of PBLs. Flow cytometer verified that cells apoptosis after 72 h exposion to costimulate activation of PBLs. CD3 and CD8 increased in tumor patients PBLs being costimulating combined with CpG ODN (P < 0. 05). CONCLUSION: Costimulating signal molecular increased, cyto kine and killer cell secreted more when activation of T cell com bined with CpG ODN. The colorectal carcinoma cell apoptosis was bring by these factors. CD3 and CD8 increased in tumor patients PBLs being costimulating combined with CpG ODN. Correlation of activation of T cell combined with CpG ODN signal molecular expression and colon cancer cell apoptosis was shown by the re sults.

T lymph cellscostimulationmembrane molecularcolon cancer cellapoptosis

方军、郭树军、李永研、李凯

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解放军第153医院普通外科,河南,郑州,450042

T淋巴细胞 共刺激 膜分子 结肠癌细胞 凋亡

2009

第四军医大学学报
第四军医大学

第四军医大学学报

CSTPCDCSCD北大核心
影响因子:0.599
ISSN:1000-2790
年,卷(期):2009.30(22)
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