炎性肠病是一种慢性非特异性肠道炎症性疾病，普遍认为免疫反应过激是致病因素之一。树突状细胞作为免疫反应的抗原呈递细胞，是免疫反应的启动者。然而对于树突状细胞在肠炎中迁移能力的变化及其机制却还不十分明确。富亮氨酸重复序列激酶2（LRRK2)是近期发现的肠炎的敏感基因，我们以前的研究发现LRRK2能调控树突状细胞(DC)内的钙池操控性钙通道，从而影响细胞内钙浓度。我们的前期结果表明：（1）肠炎模型中DC的迁移能力增加。（2）肠炎模型中DC内钙池操控性钙通道活性升高。（3）LRRK2的缺失使钙池操控性钙通道活性升高。细胞的迁移功能是依赖于钙离子浓度，我们认为LRRK2能通过调控钙池操控性钙通道影响DC迁移能力，从而参与炎性肠病的发病。本研究拟通过钙成像，膜片钳，分子生物学等试验，利用DSS诱导的肠炎模型小鼠和LRRK2敲除小鼠为模型，对此假说进行进一步验证。

Inflammatory bowel disease(IBD) is a common chronic intestinal inflammation syndrome, and abnormal immune responses are involved in its pathology. Dendritic cells(DCs) are antigen-presenting cells and considered as the first step of immune responses.However,whether the altered migration capacity of DC and its mechanism are involved in IBD remains elusive. LRRK2 is recently found to be related to the pathology of IBD. We for the first time found that LRRK2 defects facilitates intracellular calcium concentration in DCs through Store-operated calcium channel(SOCC). Our previous data showed the enhanced DCs migration and SOCE in IBD. Moreover, we already published a paper about the relationship between LRRK2 and SOCC in DCs. Given the importance of intracellular calcium concentration in the migration of DC, we propose that LRRK2 could regulate the migratory capacity via SOCC hence contributing to IBD. In the present study we aim to confirm our hypothesis in DSS-induced IBD model and LRRK2 KO mouse by the utilization of calcium imaging, patch clamp, biochemistry techniques.