幽门螺杆菌(Hp)感染致病的免疫调控机制仍不明确。我们首先发现，Hp感染下胃上皮细胞可通过上皮-免疫细胞转分化，表达树突状细胞(DC)表型- - 天然免疫分子DC-SIGN，且有别于DC表面DC-SIGN，呈现高糖基化修饰状态，具备诱发不同于DC 介导免疫逃逸的Th1促炎应答的专职免疫细胞功能。推测Hp感染下的上皮细胞DC-SIGN表达及高糖基化修饰，与区室化免疫调节有关，继而调节Th1/Th2的免疫平衡。由此，从免疫系统区室化角度并基于Hp-DC-SIGN免疫识别调控机制，研究Hp感染对DC-SIGN表达及其糖基化修饰的影响，藉此进一步阐释Hp感染下DC-SIGN表达及糖基化与病原体抗原免疫识别、免疫应答调控的关系。为探讨Hp感染及致病的免疫调控机制，提供新的理论依据及干预策略和途径。

The mechanisms of immune regulation in H. pylori related diseases are still unknown. Our previous studies have shown that gastric epithelial cells infected with H. pylori may lead to express DC-SIGN via a trans-differentiation process termed "Epithelial Immune Cell-like Transition". However, unlike on DCs, the relatively high level of glycosylation was observed in the DC-SIGN presenting on gastric epithelial cells, thus inducing a Th1-predominant host immune response in the gastric mucosa. All those above mentioned have further demonstrated that DC-SIGN in its high glycosylation state may regulate the Th1/Th2 immune balance under the control of tissue-associated immune compartments. Recognition mechanisms and immune strategies existed on H. pylori-DC-SIGN were investigated in the current study. The understanding of the relationships between DC-SIGN glycosylation induced by H. pylori and its immune recognition, response, and regulation, will provide important new insights into the pathogenesis and therapeutics for H. pylori infection.