幽门螺杆菌(H.pylori)作为胃十二指肠疾病的胞外感染病原菌，却引起胃粘膜CD8+T细胞大量聚集，数量显著高于CD4+T细胞，但具体应答机制和免疫功能尚不清楚。本课题前期研究发现：H.pylori感染促使胃上皮细胞分泌CXCL11等趋化因子，其外源性抗原可显著刺激特异性TCRαβ+CD8αβ+ T细胞应答，高表达CXCR3，且CD8敲除可导致胃粘膜细菌定植量明显增加，结果提示：CD8+T细胞可能通过交叉递呈途径和趋化因子受体介导方式进行活化与趋化，并发挥抗H.pylori感染的免疫保护，但机制尚未解析。本课题将通过H.pylori感染的细胞和小鼠模型，采用胞内共定位染色、Transwell试验、基因缺失、细胞回复、抗体阻断、过继免疫等技术，探讨CD8+T细胞经交叉递呈活化、受体介导趋化，进而发挥抗感染保护的作用与机制，将为深入解析H. pylori感染的免疫保护与损伤机制提供新的认识。

Helicobacter pylori(H. pylori) infection can induce immune response, but bacterium can not be cleaned in stomach tissue. Chronic infection of H. pylori lead to associated gastroenterological disease. As Extracellular pathogen, H. pylori infection induced more CD8+ T lymphocyte responses than CD4+ T cell in the gastric mucosa, but the immunologic function and mechanism of gastric CD8+ T cell remained unclear up to date. In our previous studies, we investigated responses characteristics of gastric CD8+ T cells in H. pylori infected mice, and found that some exogenous antigen, such as UreB, could stimulate specific CD8+ T cell responses. These gastric mucosal CD8 T lymphocytes are mainly resident memory T cells, Trm cells (CD103 +, CCR7-, CD69 +) which were classical TCRαβ+CD8αβ+. Detecting the expression of chemokine receptors, we found that gastric mucosa CD8 T cells expressed more chemokine receptors including CCR3, CCR4, CCR5 and CXCR3 in the infected mice than uninfected mice. Notably, the level of CXCR3 expression was the highest , about 60%, among detected chemokine receptors. Meanwhile, the result of protein chip showed the expression level of six kind of chemokines in the stomach tissue was more increased in the infected mice compared with the uninfected control mice (p＜0.05), including CXCL11, CCL5, CCL12, CCL22, CXCL2, CXCL13. The gastric epithelial cell line（AGS）could secrete more CXCL11 than other chemokines after H. pylori stimulation. Furthermore, there were more H. pylori colonization in the gastric mucosa in the infected CD8 knockout mice than infected wild type mice. Above some results showed that mucosal CD8+ T lymphocytes, produced by antigen presenting cells with cross-presentation for foreign antigen of H. pylori, could migrate largely into gastric mucosa through chemokine-chemokine receptor interactions, and play a protection role against H. pylori infection, but these mechanisms remained unclear. In current study, these immunological methods, such as Intracellular colocalization staining, Transwell test, CD8 knockout, Immunological recovery, antibody blocking test and adoptive immunity test, were used to investigate mechanism of cross-presentation, cell chemotaxis and protective immunity against H. pylori infection for CD8+ T cells. This research will be helpful to further understand the immunological mechanism of T cell responses against H. pylori infection and provide theory support to immunological control of H. pylori infection.