目前认为克罗恩病（CD）是由于肠黏膜免疫耐受缺失导致的黏膜-肠腔共生菌群异常作用而引起的肠道慢性炎症。研究发现SHIP-1在调节免疫耐受中起重要作用，作为SHIP-1调控因子的microRNA-155也参与多种免疫相关疾病，但microRNA-155/ SHIP-1通路在CD黏膜免疫中的作用尚不明确。我们前期研究发现CD模型小鼠出现SHIP-1蛋白的低表达，提示microRNA-155/ SHIP-1通路可能参与CD的病理生理过程，但具体机制尚需深入研究。在前期工作基础上，本课题以CD模型小鼠和CD患者肠组织为研究对象，通过分子生物学以及分子免疫学等技术，着眼于肠黏膜树突状细胞，以miR-155/SHIP-1为切入点，通过在体与离体调控miRNA-155的表达，探讨miR-155/SHIP-1通路在CD肠黏膜免疫耐受缺失中的角色，以期为揭示CD的发病机制提供依据、为CD临床防治提供靶点。

Crohn's disease, which presented as intestinal chronic inflammation, was considered as the results from uncontrolled immune response due to the lake of tolerance to luminal commensal microbiota. It was recently reported that SHIP-1, whose production was directly regulated by microRNA-155, played an important role in the immune tolerance, additionally, microRNA-155 was also found to be associated with autoimmune diseases. However, limited data about the microRNA-155/ SHIP-1 related to the pathogenesis of Crohn's disease. We previously found the decreased expression of SHIP-1 protein in the gut mucosa of Crohn's disease animal model. To further explore the pivotal role played by microRNA-155/SHIP-1 pathway in the loss of tolerance to commensal microbiota by gut mucosa with Crohn's disease, we hereby proposed a study focused on the microRNA-155/SHIP-1 pathway in CD mouse model and CD patients intestinal dendritic cells performed in vivo and in vitro, by molecular biology and immuno technology techniques. Further more,by regulation of the miRNA-155,the effects of microRNA-155/SHIP-1 pathway on the intestinal inflammation will also be explored. The result of our study may add some information for the understanding of the pathogenesis of CD and provide some therapeutic implications for the treatment of this an incurable intestinal disorder.