树突状细胞在幽门螺杆菌（Hp）感染的免疫应答中发挥重要作用。前期研究发现LECT2影响感染Hp的树突状细胞促T细胞分化的功能，且LECT2与CD209a特异性相互作用，外源性给予LECT2上调树突状细胞表面CD209a水平及其磷酸化水平，提示LECT2极可能通过调控CD209a影响感染Hp的树突状细胞的免疫功能。本项目拟在已有工作基础上，从体内和体外水平，研究LECT2对Hp感染后树突状细胞的成熟、活化和免疫反应的影响；同时确定LECT2与树突状细胞表面CD209a的相互作用，研究LECT2是否通过CD209a对感染Hp的树突状细胞的免疫功能产生影响；进一步探讨CD209a表达变化对其下游信号通路LSP1/IKKε/CYLD及Bcl3等的表达水平和活性的作用，以期明确LECT2调控CD209a影响Hp感染后树突状细胞免疫功能的分子机制。本项目为发现抗Hp治疗潜在的药物靶标奠定了基础。

Dendritic cells (DCs) play an important role in the immune response to H. pylori infection. Our studies demonstrate that LECT2 could alter the DC-polarized Th1/Th2 response upon H. pylori infection, and LECT2 could interact with CD209a expressed on DCs and exogenous administration of LECT2 could up-regulate the level of CD209a and its phosphorylation, which suggested that LECT2 may affect the immune function of DCs infected with H. pylori by regulating CD209a. In this project, we try to analyze the effect of LECT2 on maturation, activation and immune response of DCs and whether these effects are mediated through CD209a in vivo and in vitro. In addition, we will examine the effect of CD209a on LSP1/IKKε/CYLD signaling pathways and downstream Bcl3 pathways, in order to determine how LECT2-induced CD209a regulate immune function of DCs upon H. pylori infection. Our findings will contribute to identify potential drug targets for H. pylori eradication therapy.