趋化因子MCP-3基因和B7基因共转染诱导抗大肠癌主动免疫

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-/B＋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，共转染的细胞作为疫苗治疗已形成的肿瘤有一定的疗效。

Co-Transfection of Colorectal Cancer Cells with Chemokine MCP-3 Gene and B7 Gene to Induce Anti-Tumor Immunity

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.