The etiology of autoimmune thyroid disease: A story of genes and environment

被引：261

作者：

Tomer, Yaron ^{[1
,2
]}

Huber, Amanda

机构：

[1] Univ Cincinnati, Div Endocrinol, Vontz Ctr Mol Studies, Coll Med, Cincinnati, OH 45267 USA

[2] Univ Cincinnati, Coll Med, Cincinnati VA Med Ctr, Cincinnati, OH 45267 USA

来源：

JOURNAL OF AUTOIMMUNITY | 2009年 / 32卷 / 3-4期

关键词：

Graves' Disease; Hashimoto's thyroiditis; Genes; Environment; THYROTROPIN RECEPTOR GENE; SINGLE-NUCLEOTIDE POLYMORPHISM; CHRONIC HEPATITIS-C; INTERFERON-ALPHA THERAPY; LYMPHOID TYROSINE PHOSPHATASE; STRESSFUL LIFE EVENTS; MHC CLASS-II; HCV CHRONIC HEPATITIS; TOXIC NODULAR GOITER; LOW IODINE INTAKE;

D O I：

10.1016/j.jaut.2009.02.007

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Autoimmune thyroid diseases (AITDs), including Graves' disease (GD) and Hashimoto's thyroiditis (HT) are prevalent autoimmune diseases, affecting up to 5% of the general population. Autoimmune thyroid diseases arise due to complex interactions between environmental and genetic factors. Significant progress has been made in our understanding of the genetic and environmental triggers contributing to AITD. However, the interactions between genes and environment are yet to be defined. Among the major AITD susceptibility genes that have been identified and characterized is the HLA-DR gene locus, as well as non-MHC genes including the CTLA4, CD40, PTPN22, thyroglobulin, and TSH receptor genes. The major environmental triggers of AITD include iodine, medications, infection, smoking, and possibly stress. Recent data on the genetic predisposition to AITD lead to novel putative mechanisms by which the genetic-environmental interactions may lead to the development of thyroid autoimmunity. Published by Elsevier Ltd.

引用

页码：231 / 239

页数：9

共 186 条

[71] Association between a C/T polymorphism in Exon 33 of the thyroglobulin gene is associated with relapse of graves' hyperthyroidism after antithyroid withdrawal in Taiwanese [J].