炎症性肠病（Inflammatory bowel disease, IBD)是一类病因及发病机制尚未完全明确的特殊肠道炎症。我们前期的研究证明：维生素D(VD)及其受体（VDR）能够促进肠黏膜屏障功能，抑制IBD发生。肠道微褶皱细胞（microfold cell, M细胞）是肠粘膜免疫启动的关键，近期我们又发现VD/VDR能够影响M细胞的形成和功能，抑制IBD，这预示着可能存在新的调控机制：VD/VDR--M细胞--肠黏膜屏障-- IBD。本项目将采用肠上皮细胞、转基因小鼠（VDR敲除和VDR肠上皮特异性敲除小鼠等）和临床样本，结合分子生物学，细胞生物学和IBD小鼠模型等方法，研究VD/VDR调控M细胞的作用及机制，阐明VD/VDR保护肠黏膜屏障、参与区域免疫调节、防御炎症性肠病的新机制，为临床预防、诊断和治疗炎症性肠病的应用研究提供新策略及理论依据。

Inflammatory bowel disease (IBD) is a type of special intestinal inflammation. Our previous studies demonstrated that vitamin D and its receptor promotes intestinal mucosal barrier function and inhibits IBD. Recently, we found that VD / VDR can affect the formation and function of microfold cell (M-cell), the key of gut mucosal immune activation. Suggesting that there may be a regulatory pathway: VD / VDR - M cells - intestinal mucosal barrier - IBD. The project will use intestinal epithelial cells, mouse model（VDR knockout and VDR intestinal specific knockout mice）and clinic samples, through a variety of molecular biology, cell biology and IBD mouse models and other methods to clarify the role of VD / VDR regulating M cells and its mechanism ，to explore the new mechanism of VD / VDR protective intestinal mucosal barrier, involving in regional immunomodulation, prevention of inflammatory bowel disease， and provide new Strategy and theory for the clinical prevention, diagnosis and treatment of inflammatory bowel disease application research.