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作 者:刘然义[1] 熊宇芳[2] 屈伸[2] 尤颖健[2] 邓耀祖[2]
机构地区:[1]中山医科大学肿瘤防治中心生物治疗室,广州510060 [2]同济医科大学生化教研室,武汉430030
出 处:《癌症》1999年第5期562-565,共4页Chinese Journal of Cancer
基 金:国家教委基金!资助课题(NO.JW9307)
摘 要:目的:初步探讨弱免疫原性肿瘤细胞导入CD80 基因后免疫源性是否增强,以及肿瘤免疫原性与细胞表面分子的关系。方法:通过脂质体介导将CD80 基因导入小鼠黑色素瘤B16 细胞后,利用SABC 法检测CD80 的表达;MTT 法测定肿瘤细胞体外增殖能力;将肿瘤细胞接种至同源小鼠皮下后观察成瘤期、荷瘤小鼠存活期及肿瘤结节生长速度;在同源淋巴细胞肿瘤细胞混合培养( MLTCs) 后,通过测定淋巴细胞增殖指数( MTT 法) 和CTL 杀伤活性(LDH 释放改良法) 检测肿瘤细胞的免疫原性。结果:CD80 基因转染的B16 细胞中存在CD80 的稳定表达;与野生型B16 细胞和模拟转染的B16 细胞比较,CD80 转染的B16 细胞体外生长速度无明显变化( P > 0-05) ,体内生长速度明显减慢( P< 0-05) ,体外刺激淋巴细胞增殖和诱导CTLs 的能力明显增强( P< 0-05) 。结论:弱免疫原性肿瘤细胞导入CD80 基因可增强免疫原性,其作用强弱与肿瘤细胞表达MHC 及ICAM1 等分子的状况有关。Objectives:To investigate the effects of the CD80 costimulatory molecule expression on the immunogenicity and biological characteristics of poorly immunogenic B16 melanoma cells, explore the relationship between the immunogenicity of tumor cells and cell surface molecules. Methods:Human CD80 cDNA was transfected into B16 melanoma cells by lipofectin mediated gene transfer before the expansion of tumor cells were tested by MTT method in vitro;C57BL/6 mice were inculated subcutaneously either mock transfected B16 cells (B16 neo)or CD80 transfected B16 cells (B16 CD80),then the latency,survival times and tumor mass growth were investigated.The lymphocytes were examined for both proliferation indices (PI) and specific cytotoxic activity by MTT method and improved LDH releasing method,after syngenic Mixed Lymphocyte tumor cultures (MLTCs). Results:In the B16 CD80 cells,in which CD80 expression were detected by SABC method, demonstrated slower growth rate than B16 neo Clles in vivo (P< 0 05) , though they didn't in vitro.Compared with B16 wt and B16 neo cells, B16 CD80 cells more effectively induced the proliferation of effector lymphocytes and the generation of specific lytic activity against B16 wt cells. Conclusions:The CD80 (B7 1) expression in poorly immunogenic tumor cells can increase their immunogenicity and decrease their tumorigenicity,the effects are associated with the expression of ICAM 1 and MHC molecules on tumor cells surface.
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