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为了进一步研究细胞因子基因转染后肿瘤细胞体内致癌原性、免疫原性变化的分子 机制，将ＩＬ－２、ＩＬ－４ 基因转染入Ｂ１６黑色素瘤细胞，观察了其体内接种后致瘤原性变化，通过 ＦＡＣＳ法检测了其细胞表面粘附分子－１（ＩＣＡＭ－１）的表达水平，分析了其细胞表面 ＩＣＡＭ－１表达水 平以及它们与肿瘤细胞对ＬＡＫ、ＣＴＬ等免疫效应细胞杀伤敏感性变化的关系。结果表明，ＩＬ－２、ＩＬ－ ４基因转染后Ｂ１６细胞体内致瘤原性明显降低，其细胞表面ＩＣＡＭ－１的表达高于野生型Ｂ１６细胞， 且对ＬＡＫ、ＣＴＬ细胞的杀伤敏感性增加。抗ＩＣＡＭ－１单抗可以阻断ＩＬ－２、ＩＬ－４基因转染后Ｂ１６细 胞对ＬＡＫ、ＣＴＬ杀伤敏感性的增强效应。表明细胞因子基因转染后Ｂ１６细胞体内致瘤原性改变除 与其诱导或增强机体的抗肿瘤免疫反应有关外，还与细胞表面ＩＣＡＭ－１分子的表达增加从而使其 对免疫效应细胞的杀伤敏感性增强有关。
In order to further study the molecular mechanism of the in vivo carcinogenicity and immunogenicity of tumor cells after transfection of cytokine genes, the IL-2 and IL-4 genes were transfected into B16 melanoma cells and their in vivo tumorigenicity was observed. Changes in the expression of ICAM-1 were detected by FACS. The expression of ICAM-1 on the cell surface and their sensitivity to killing of LAK, CTL, and other immune effector cells were analyzed. The relationship between sexual changes. The results showed that the in vivo tumorigenicity of B16 cells was significantly decreased after IL-2 and IL-4 gene transfection. The expression of ICAM-1 on the cell surface was higher than that of wild type B16 cells, and the sensitivity to killing of LAK and CTL cells was increased. . The anti-ICAM-1 monoclonal antibody can block the enhanced effect of IL-2 and IL-4 gene transfection on the killing susceptibility of B16 cells to LAK and CTL. It was shown that the in vivo tumorigenicity of B16 cells transfected with cytokine genes was not only related to its induction or enhancement of the body’s anti-tumor immune response, but also to the increased expression of ICAM-1 molecules on the cell surface so that it was sensitive to the killing of immune effector cells. Related to sexual enhancement.