IL-37通路在多发性硬化发病机制中的保护性作用研究

项目名称： IL-37通路在多发性硬化发病机制中的保护性作用研究

项目编号： No.81200920

项目类型： 青年科学基金项目

立项/批准年度： 2013

项目学科： 神经系统疾病、精神疾病

项目作者： 汪鸿浩

作者单位： 安徽医科大学

项目金额： 23万元

中文摘要： 多发性硬化是一种常见的中枢神经系统自身免疫性疾病，以CD4+T细胞激活和炎症因子释放，损伤胶质细胞，导致神经纤维髓鞘脱失为主要病理过程，是造成青年人群丧失劳动能力的重要原因。MS的发病机制至今未明，目前无特效的治疗方法，给社会和家庭带来沉重的负担。IL-37是白细胞介素1家族的新成员，在最近的研究中显示有IL-37可以显著减少各种炎症因子的释放，还可能通过Smad3途径可以影响CD4+T细胞亚群的激活、分化。本课题旨在依据申请者多年对MS的免疫学机制研究基础上，通过动物实验和体外细胞培养验证IL-37对Th1、Th17、Treg细胞的分化调节及其对炎症因子的释放的影响，直观的展示IL-37通路对MS模型的保护性作用，通过临床研究统计MS患者复发期和缓解期血清、脑脊液IL-37水平变化和扩展残疾状况评分、CD4+T细胞亚群以及炎症因子的相关性，为IL-37的临床应用提供理论依据。

中文关键词： 多发性硬化；实验自身免疫性脑脊髓炎；白细胞介素37；CD4+T细胞；免疫调节

英文摘要： Multiple sclerosis (MS) is one of the most common auto-immune diseases in central nervous system (CNS). The demyelination found in MS is thought to be caused by an autoimmune process, in which activating CD4+T cell and releasing inflammatory cytokines will lead to glial damage. MS is one of most important reasons for youth population lost their ability to work. The pathogenesis of MS is still unclear. There is no effective way to cure MS. MS place heavy burdens on the patients, the families, and the society. IL-37 is a new member of the interleukin 1 family. In Recent studies，IL-37 is shown can inhibit the release of inflammatory cytokines in the inflammatory process and regulate CD4+T cell immunity through Samd3 pathway. Based on the applicant's research about the immunological mechanisms of MS, in this project, we use animal experiments and vitro cell culture to prove the protective effect of IL-37 pathway in MS model though regulate the differentiation of Th1, Th17 and Treg cells, and reduce the production of inflammatory cytokines. We also statistics IL-37 levels in serum and cerebrospinal fluid during relapse and remission.To provide the theoretical basis for the clinical application of IL-37, we explore the correlation among IL-37 levels, expanded disability status scale，EDSS) scales, CD4+T cell subsets an

英文关键词： Multiple sclerosis；experimental autoimmune encephalomyelitis；interleukin 37；CD4+ T cells；Immunomodulatory