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本文观察了协同刺激分子B7-1某因导入小鼠EL-4淋巴瘤细胞后在小鼠体内诱导的抗瘤效应.结果表明,逆转录病毒(PLXSN)载体重组的小鼠B7-1基因表达质粒导入小鼠EL-4淋巴瘤细胞,经有限稀释法克隆后获得高表达的B7-1~+EL-4细胞.B7-1~+瘤细胞的形态,体外增殖能力及MHC Ⅰ类分子表达水平与野生型肿瘤细胞无显著差别,但致瘤性显著降低,用野生型肿瘤致死剂量接种C57BL/6小鼠完全排斥.同时免疫原性明显增强,以X-线灭活的B7-1~+肿瘤细胞免疫后小鼠获得了对随后致死剂量野生型细胞攻击的免疫保护作用.以X-线灭活的肿瘤细胞作为瘤苗进行实验性免疫治疗,对早期(接种7天)形成的肿瘤有一定的治疗效果,但时晚期(接种14天)肿瘤.B7-1和B7-1~+瘤细胞都未显示出明显的治疗效果.上述结果提示肿瘤细胞表达B7-1分子可有效激发机体的抗肿瘤免疫应答.
In this study, we observed the anti-tumor effect of the co-stimulatory molecule B7-1 which was induced in mice by incorporation into mouse EL-4 lymphoma cells. The results showed that the retroviral vector (PLXSN) recombinantly expressed mouse B7-1 gene. Plasmids were introduced into mouse EL-4 lymphoma cells and cloned by limiting dilution method to obtain highly expressed B7-1~+EL-4 cells. B7-1~+ tumor cell morphology, in vitro proliferation and MHC class I molecule expression There was no significant difference between wild-type tumor cells and wild-type tumor cells, but the tumorigenicity was significantly reduced. C57BL/6 mice were completely rejected by lethal doses of wild-type tumors, and the immunogenicity was significantly enhanced, and the B7-1 was inactivated by X-rays. After immunization with tumor cells, the mice received immunoprotection against subsequent lethal doses of wild-type cells. The X-ray-inactivated tumor cells were used as tumor vaccines for experimental immunotherapy and the early (7-day inoculation) tumors were formed. There is a certain therapeutic effect, but late (inoculation 14 days) tumors. B7-1 and B7-1 ~ + tumor cells did not show obvious therapeutic effect. The above results suggest that tumor cells expressing B7-1 molecules can effectively stimulate the body Anti-tumor immune response.