随着胃癌肿瘤微环境相关基础研究的深入开展，以及免疫检查点抑制剂的临床应用，胃癌肿瘤浸润免疫细胞的研究越来越引起关注。但是目前多项临床研究表明PD-1/PD-L1免疫检查点抑制剂在胃癌患者中的疗效有限。本项目通过生物信息学分析，筛选鉴定出一批与胃癌肿瘤微环境中CD8+ T细胞浸润呈高度正相关的免疫抑制因素，包括Treg细胞的标志基因、各类免疫检查点及趋化因子。进一步实验表明CCL19/CCR7信号轴对Treg细胞有明显趋化作用，并与胃癌患者预后呈显著负相关。由此推测，CCL19/CCR7信号轴通过趋化Treg细胞向胃癌肿瘤微环境浸润，从而抑制CD8+ T细胞的功能，促进了胃癌免疫逃逸。本课题将通过一系列细胞和动物模型水平的分子、生化及免疫学实验，探究CCL19/CCR7信号轴在胃癌免疫微环境中发挥的作用及机理。

With the further study on tumor microenvironment in gastric cancer and application of immune checkpoint inhibitors in clinical treatments, research work on tumor infiltrating immune cells is attracting more and more attention. However, several clinical researches at present indicate that PD-1/PD-L1 inhibitors have limited efficacy in gastric cancer. We have screened a series of immunosuppressive factors that are highly correlated with tumor infiltrated CD8+ T cells in gastric cancer, including Treg cell signature genes, immune checkpoints and chemokines. Further experiments demonstrate that CCL19/CCR7 has obvious chemotacic effect on Treg cells and indicates poor prognosis in gastric cancer. Thus we propose hypothesis that CCL19/CCR7 mediates Treg cells infiltration and then inhibits function of CD8+ T cells, resulting in immune escape in gastric cancer. We plan to facilitate biochemical, molecular and immunological researches to further identifying molecular mechanism of CCL19/CCR7 in immune microenvironment in gastric cancer.