黑斑息肉综合征(PJS) 以肠道息肉病为特征，癌变风险高，危害大。LKB1基因突变是主要致病因素，LKB1在多种细胞的选择性缺失皆可导致PJS发生，但PJS发生分子机制不是十分清楚。树突状细胞（DC）是体内功能最强的专职抗原递呈细胞，LKB1在DC的缺失是否导致PJS未见报道。我们发现DC缺失LKB1使大于6月小鼠全部发病，肠道见息肉，无明显炎症，推测DC缺陷LKB1导致其下游关键信号转导分子产生变化，使相关效应分子的水平发生改变，导致PJS息肉的产生。我们以研究胃肠道DC的LKB1信号对PJS发病的影响及机制为核心科学问题，以现代细胞免疫学和分子免疫学方法为核心技术，联合应用转基因和基因敲除小鼠，研究稳态下胃肠道DC缺失LKB1以后，对PJS发生发展的影响，探明LKB1下游的关键信号传导分子，并找到相关效应分子，为阐明PJS发病的细胞和分子机制做铺垫，为研制PJS的防治手段提供理论基础。

Peutz–Jeghers syndrome (PJS), a cancer predisposition syndrome characterized by benign gastrointestinal (GI) polyps, is caused by a germline mutation in STK11, the gene that encodes the tumor suppressor LKB1. Patients with PJS show an increased risk of developing cancer at relatively young ages. Multiple substrates and pathways Lkb1 has been found to be involved, however, it is unclear which of these are critical for suppressing GI polyposis. Importantly, the cell types and signaling pathways underlying polyposis formation are still not fully understood. DC are professional antigen-presenting cells and reside in almost all tissues where they function as immune sentinels. It is not clear whether DC is sufficient to promote GI polyposis when Lkb1 is deleted. To elucidate the role of LKB1 in DC, we bred mice bearing floxed alleles of Lkb1 against animals carrying Cre recombinase under CD11c promoter control. Here, we demonstrated that DC-specific deletion of Lkb1 results in fully penetrant polyposis in mice (developed at 120 days of age). We hypothesized that Lkb1-mediated changing of key signal transduction molecules in DC regulates the level of effectors, which might be essential for controlling gastrointestinal polyps prognosis. In this study, with modern cellular, molecular immunological methods and transgenic mice strains, we expect to demonstrate the downstream molecular mechanism regulated by the LKB1 signaling in DC, and to identify the effector. This may provide a new target for the prevention and treatment of PJS. molecular mechanism regulated by the LKB1 signaling in DC, and to identify the effector. This may provide a new target for the prevention and treatment of PJS.