摘要
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 elucidate the molecular mechanisms which involve in changes of the tumorigenicity of cytokine gene-transfected tumor cells, we transfected IL-2 gene,IL-4 gene into B16 melanoma cells, and then observed their tumorigenicity in vivo. The expression level of ICAM-1 were also detected by FACS method. Sensitivities of the cytokine gene transfected B16 cells to LAK,CTL cytotoxicity were compared with that of the wild-type B16 cells. The results demonstrated that both IL-2 gene and IL-4 gene-transfected B16 cells have more increased ICAM- expression than the wild-type B16 cells. These cytokine gene modified B16 cells become more sensitive to LAK or CTL cytotoxicity, and that can be abolished by anti-ICAM-1 monoclonal antibody. The present result suggested that the decreased tumorigenicity of the IL-2 gene,IL-4 gene transfected B16 melanoma cells can be attribute to not only their increased antitumor immunity of the host, but also to the increased sensitivitiy to effector cells by increased ICAM-1 expression.
出处
《中国免疫学杂志》
CAS
CSCD
北大核心
1996年第1期20-24,共5页
Chinese Journal of Immunology
基金
国家自然科学基金!(39470800)
军队八五攻关项目
