自身免疫甲状腺炎（AIT）是内分泌系统常见病之一，患病人群约占人口的10-12%。目前普遍认为AIT是环境和遗传因素共同作用的器官特异性自身免疫病，但是具体发病机制尚不明确。免疫代谢异常是近年来进展较快的领域之一，尤其在自身免疫病发病机制中的作用方面取得很大进展，而AIT方面的报告甚少。本项目以免疫代谢异常中糖酵解异常及其相关信号通路为主要研究内容，① 研究免疫细胞糖酵解激活及其调节机制异常在人类AIT发生发展中的作用，通过干预手段抑制糖酵解激活，延缓AIT发展进程或减轻病情，为寻找AIT新的治疗靶点提供线索；②研究环境因素（碘过量）激活免疫细胞糖酵解的机制，干预或纠正相关环境因素抑制免疫细胞糖酵解形成，为制定有效的公共卫生疾病预防策略提供理论基础。

Autoimmune thyroiditis（AIT）is a common disease in endocrine system which accountfor 10-12% of population. It has been accepted widely that AIT is an organ-specific autoimmune disease caused by genetic background and environment factors. However the mechanism is not verified. The field of immunometabolic is developing very quickly recent years, especially in autoimmune disease except for AIT. This project is going ①to investigate the immunometabolic (glycolysis) in patient with AIT, verifying the immunometabolic involved in occurrence and development of AIT, proving inhibition of the immunometabolic can delay or alleviate AIT, providing clues for new therapeutic targets and treatment strategies; ②to understand the mechanism of environmental factors (excessive iodine intake) that activate glycolysis, proving that intervention or correcting related environmental factors can inhibit formation of glycolysis，providing the theoretical basis for disease prevention strategy.