流行病学研究提示，碘摄入增加促进自身免疫性甲状腺疾病（AITD）尤其桥本氏甲状腺炎（HT）的发生多见于患有某些疾病背景的个体上；而完全正常的个体，碘摄入增加很少诱发AITD。据此推测碘摄入增加可能通过和遗传因素的相互作用，如影响碘吸收排泄或AITD的易感基因等，来促进AITD的发生。本项目主要的研究内容是在课题组前期已经完成的3,052例个体GWAS基因分型的基础上，识别鉴定影响血碘浓度的易感基因；并进一步研究识别鉴定的使血碘浓度升高或降低的易感基因的基因型，是否是自身免疫性甲状腺疾病Graves’病（GD）或桥本氏甲状腺炎（HT）的致病易感基因型，从而明确血碘升高或降低和GD或HT发生之间的关系。同时，我们还将以课题组收集的10,000例流行病学人群为研究对象，研究碘摄入量与AITD致病易感基因之间的相互作用，在其发生中的作用，从而明确碘促进AITD发生的可能分子靶点。

Epidemiological studies have suggested that increased iodine intake enhanced the incidence of autoimmune thyroid disease (AITD) especially Hashimoto's thyroiditis (HT) that mostly occurs in the individuals suffering from certain diseases with susceptiblity to AITD. However, , increase of the iodine intake rarely induced AITD in normal individuals. Based on the data, we hypothesized that increased iodine intake may accelerate the occurrence of AITD, mediated by interaction between iodine with inherited factors, such as the susceptible genes influencing iodine absorption and excretion or the susceptibility genes to AITD. The main aims of the project are to identify susceptibility genes influencing the serum iodine concentration base on our previous GWAS data collected from 3,052 individuals and further investigate the association of the genotypes of these susceptibility genes, which increased or decreased the circulation concentration of iodine, with Graves' disease (GD) or Hashimoto's thyroiditis (HT), in order to elucidate the roles of the genotypes of the susceptibility to the circulation concerntration of iodine in the incidence of GD or HT. The second aim of the project is to study the roles of the interaction of iodine intake and susceptibility genes of AITD in the pathogenesis of AITD built on 10,000 population samples collected from Chongming island, Shanghai by our group. These data will underline the molecular targets which mediated the increase iodine intake inducedAITD.