目的:探讨趋化因子MCP-3（monocyte chemotactic protein-3）和B7基因共转染诱导抗大肠癌主动免疫的可能性。方法:用脂质体将小鼠MCP-3和B7（B7.1）基因导入小鼠大肠癌CMT93细胞，G418筛选抗性克隆，RT-PCR检测B7和MCP-3的表达，趋化实验检测MCP-3的功能。体内实验观察基因修饰瘤细胞(CMT93/B7+MCP-3)的成瘤性、免疫小鼠后所诱导的针对CMT93的免疫保护及其作为疫苗治疗已形成肿瘤的疗效。结果: RT-PCR检测发现CMT93/B7+MCP-3瘤细胞有B7和MCP-3的表达，而且所表达的MCP-3有良好的趋化活性。CMT93/B7+MCP-3的成瘤性显著下降(P<0.01)。经CMT93/B7+MCP-3免疫的小鼠获得对CMT93的免疫保护(P<0.05)。作为疫苗CMT93/B7+MCP-3能抑制接种早期肿瘤的生长。结论:共转染MCP-3和B7基因能有效诱导抗大肠癌主动免疫，共转染的瘤细胞作为疫苗治疗已形成的肿瘤有一定的疗效。

Objective: To evaluate the possibility of the anti-tumor immunity induction by co-transfecting the colorectal cancer cells with chemokine MCP-3 and B7 gene. Methods: Mouse MCP-3 and B7(B7.1) genes were transduced into mouse colorectal cancer CMT93 cells using Liposome. G418-ressistant clones were selected. MCP-3 and B7 mRNA expression was detected by RT-PCR. Chemotactic activity of MCP-3 was measured by chemotaxis assay. The tumoregericity of gene transfectants (CMT93/B7+MCP-3) was detected by in vivo experiments. The immune protection against rechallenged CMT93 in the mice primed by CMT93/B7+MCP-3 was observed, and the effect of CMT93/B7+MCP-3 as vaccine to treat established tumors in the early stage was detected by in vivo experiments as well. Results:CMT93/B7+MCP-3 expressed MCP-3 and B7 mRNA, but control groups not expressed. The secreted MCP-3 in the cell culture supernatant possesses the chemotatic activity. in vivo experiments showed that the tumorigenicity of CMT93/B7+MCP-3 was reduced significantly (P<0.01), All mice primed by CMT93/B7+MCP-3 got system immunity against the rechallenged CMT93 (P<0.05). And CMT93/B7+MCP-3 as vaccine retarded the growth of the tumors from the early stage of CMT93.Conclusion: The co-transfection of MCP-3 gene and B7 gene promotes the induction of anti-colorectal cancer immunity, and co-transfectant as vaccine is effective to treat the established tumors.