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目的探讨赋予肝癌细胞第二信号分子B7.1、增强癌细胞与淋巴细胞之间的识别与激活作用 ,从而达到增强淋巴细胞对肝癌细胞的杀伤或抑制作用。方法利用逆转录方法 ,转染B7.1分子至包装细胞系PA317。筛选获得高滴度的克隆后 ,以病毒上清感染肝癌细胞 ,使其表达B7.1分子 ,最后以LDH释放法测定LAK细胞的细胞毒活性。结果肝癌细胞可稳定表达B7.1分子 ,阳性率达94.3% ,未转染的细胞无表达 ;其所诱发的LAK细胞的细胞毒活性明显强于未转染的肝癌细胞组(P<0.01)。结论B7.1分子在淋巴细胞与癌细胞之间的识别过程中起着重要作用 ,可介导淋巴细胞对癌细胞的粘附和识别 ,从而增强淋巴细胞的杀伤作用。这一结果可为今后进一步深入研究B7.1的作用机制 ,以及与其它细胞因子、粘附分子的相互作用打下基础。
Objective To investigate whether the second signal molecule B7.1 is conferred on liver cancer cells and enhance the recognition and activation between cancer cells and lymphocytes so as to enhance the killing or inhibiting effect of lymphocytes on liver cancer cells. Methods B7.1 transfectants were transfected into packaging cell line PA317 by reverse transcription method. After screening for high titer clones, the virus supernatant was used to infect hepatoma cells to express B7.1 molecules. Finally, the cytotoxic activity of LAK cells was assayed by LDH release assay. Results The hepatoma cells stably expressed B7.1, the positive rate was 94.3%, and the untransfected cells had no expression. The induced cytotoxicity of LAK cells was significantly higher than that of untransfected HCC cells (P <0.01) . Conclusion The B7.1 molecule plays an important role in the recognition of lymphocytes and cancer cells, and can mediate the adhesion and recognition of lymphocytes to cancer cells, thereby enhancing the killing effect of lymphocytes. This result can lay a foundation for further study on the mechanism of action of B7.1 and the interaction with other cytokines and adhesion molecules in the future.