中文摘要：

IL-17是Th17细胞产生的诱导炎症反应的早期启动因子,IL-6是活化的T细胞和成纤维细胞产生的一种多效的促炎性细胞因子,都参与溃疡性结肠炎结肠癌的发生发展过程.通过DSS诱导小鼠慢性结肠癌模型,利用IL-17及IL-6基因敲除小鼠,分析了IL-17、IL-6在肠癌模型中对肿瘤的形成,对机体免疫反应过程中主要T细胞亚型及细胞因子的影响.结果显示,敲除IL-17能加重慢性肠炎诱导的结肠癌.这种加剧作用并不是通过影响T细胞的激活,而是可能通过上调CD8＋T细胞的IFN-γ加重慢性肠炎进而促进肠癌的发生.敲除IL-6对肠癌表型影响不显著,但对T细胞的功能的影响与IL-17类似.该工作为深入探讨IL-17、IL-6对慢性结肠癌发生的调控机制奠定了一定的基础.

英文摘要：

IL-17 is an early inflammatorypromoter of Th17 cells,IL-6is a pleiotropic pro-inflammatory cytokinederived from activated T cells and fibroblasts,both of them are involved in the development ofcolitis-associated carcinogenesis（CAC）.In thisstudy,we examined the tumor formation and the change of major T cell subsets and cytokinesduring the procession of DSS induced experimental CAC mousemodel,usingIL-17 KO and IL-6KO mice.The results showed,ablation of IL-17 aggravates the colon cancer induced by chronic colitis.This aggravated effect is not due to T cellsactivation,but may occur through up-regulation of IFN-γin CD8＋T cells which aggravates chronic colitistopromote cancer.Ablating IL-6has no significant effect on tumor progression,but the effect of IL-6on T cell function is similar to Ablating IL-17.This work lays the foundation for exploring the regulatory mechanism of IL-17 and IL-6on development of colitis-associated carcinogenesis.