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现已知CTL对肿瘤细胞杀伤主要通过穿孔素及(Fas-L)两个途径.最近有研究表明:过量bcl-2基因表达能拮抗部分CTL对肿瘤的杀伤活性.然而对bcl-2拮抗CTL的杀伤活性的分子机制尚不明确.为此,我们应用抗Fas单抗模拟Fas-L的杀伤作用来研究bcl-2对Fas-L诱导肿瘤细胞凋亡途径的影响,从而了解bcl-2基因在淋巴瘤癌变过程中逃避机体免疫监控的作用机制.
CTL is known to kill tumor cells mainly through perforin and (Fas-L) pathways. Recent studies have shown that: excessive bcl-2 gene expression can antagonize the killing activity of some CTLs against tumors. However, it antagonizes CTL against bcl-2. The molecular mechanism of the killing activity is not yet clear. To this end, we used an anti-Fas monoclonal antibody to mimic the killing effect of Fas-L to study the effect of bcl-2 on Fas-L-induced apoptosis in tumor cells and to understand the bcl-2 gene. The role of evasive immune monitoring in the process of lymphoma carcinogenesis.