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目的 :研究B7基因修饰的肿瘤细胞诱导抗大肠癌CTL的活化。方法 :采用电击法将B7基因导入小鼠大肠癌细胞CMT93 ,G418筛选阳性克隆 ,免疫组化显示B7分子有高效表达 ,B7 +CMT93(CMT93 -B7)接种于C57BL/6小鼠背部皮下 ,其致瘤性显著下降 (P<0 01) ;CMT93 -B7致敏的小鼠对野生型瘤细胞具有免疫保护作用(P<0 05) ;用CMT93和CMT93 -B7细胞分别经腹腔免疫小鼠 ,得到腹腔浸润淋巴细胞及致敏脾细胞 ,MTT法进行体外杀伤实验。结果 :CMT93 -B7诱导的CTL(cytotoxicTlymphocyte)对CMT93的杀伤活性显著高于野生型CMT93诱导的CTL对相同靶细胞的杀伤活性(P<0 05) ,并且CMT93 -B7诱导的CTL对CMT93 -B7的杀伤率显著高于对野生型CMT93的杀伤率 (P<0 05)。结论 :B7分子有效地促进抗大肠癌CTL的活化 ,在CTL的效应阶段B7分子也发挥重要作
Objective: To study the B7 gene modified tumor cells induced anti-colorectal cancer CTL activation. Methods: B7 gene was transfected into mouse colorectal cancer cell line CMT93 by electroporation. Positive clones were screened by G418. Immunohistochemistry showed that B7 was highly expressed. B7 + CMT93 (CMT93 -B7) was inoculated subcutaneously in C57BL / 6 mice The tumorigenicity was significantly decreased (P <0.01). CMT93-B7-sensitized mice had protective immunity against wild-type tumor cells (P <0.05). The mice were immunized intraperitoneally with CMT93 and CMT93- Obtained peritoneal infiltration of lymphocytes and sensitized splenocytes, MTT method for in vitro killing experiments. RESULTS: Cytotoxic T lymphocyte (CTL) induced by CMT93-B7 was significantly more cytotoxic to CMT93 than CTL induced by wild-type CMT93 (P <0.05), and CTL induced by CMT93-B7 had no cytotoxic effect on CMT93-B7 Was significantly higher than that of wild-type CMT93 (P <0.05). CONCLUSIONS: B7 molecules effectively promote CTL activation in anti-colorectal cancers, and B7 molecules also play an important role in the effector phase of CTL