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γ干扰素(IFN-γ)可通过增加MHCⅠ类分子或其它机制增强多种肿瘤的转移能力,而将T细胞共刺激分子B7基因导入肿瘤细胞能增强机体免疫系统对肿瘤的攻击。本文以Lipofectamine转染法将小鼠B7-1(mB7-1)基因导入B16黑色素瘤低转移株,导入空载体(只含neo基因)的B16细胞作对照。亲本B16细胞和基因转导细胞(B16-B7-1和B16-neo)经100U/ml IFN-γ预处理36小时后进行实验性肺转移试验,同时流式细胞分析细胞表面MHCⅠ类和Ⅱ类分子的表达。结果发现,IFN-γ预处理明显增强B16和B16-neo细胞的肺转移能力,而经IFN-γ预处理的B16-B7-1细胞转移能力并不增强,其实验性肺转移结节数与未经处理的对照组无差别。流式细胞分析显示IFN-γ预处理使B16、B16-neo和B16-B7-1三种细胞的MHCⅠ类(H-2K~b和H-2D~b)分子均明显增高,但IFN-γ增加B16-B7-1细胞MHCⅡ类分子I-A~b表达程度显著高于其它两种细胞。结果表明,转导B7-1基因可降低IFN-γ诱导的B16细胞转移能力,MHCⅡ类分子表达增高可能在其中起一定作用。
Interferon-gamma (IFN-γ) can enhance the metastatic ability of many tumors by increasing MHC class I molecules or other mechanisms, and introduction of the T cell co-stimulatory molecule B7 gene into tumor cells can enhance the immune system’s attack on tumors. In this study, mouse B7-1 (mB7-1) gene was introduced into B16 melanoma low metastatic strain by Lipofectamine transfection method, and empty vector (neo gene only) B16 cells were used as control. Parental B16 cells and gene transduced cells (B16-B7-1 and B16-neo) were treated with 100 U/ml IFN-γ for 36 hours and subjected to an experimental lung metastasis assay. Flow cytometric analysis of cell surface MHC class I and II was performed. Molecular expression. The results showed that IFN-γ pretreatment significantly enhanced the lung metastasis capacity of B16 and B16-neo cells, but the transfer ability of B16-B7-1 cells pretreated with IFN-γ was not enhanced, and the number of experimental pulmonary metastases was not significant. There was no difference in the untreated control group. Flow cytometry analysis showed that IFN-γ pretreatment increased the number of MHC class I (H-2K~b and H-2D~b) molecules in B16, B16-neo and B16-B7-1 cells, but IFN-γ The expression of MHC class II IA~b in B16-B7-1 cells was significantly higher than that in the other two types of cells. The results showed that transduction of B7-1 gene can reduce the ability of IFN-γ-induced B16 cell metastasis, and increased expression of MHC class II molecules may play a role in this.