Abstract
Hashimoto's thyroiditis (HT) is one of the most prevalent autoimmune diseases provoked in genetically susceptible individuals by several triggers. Immune-regulatory genes such as HLA, CTLA-4, and PTPN22 play a major role in the pathogenesis of autoimmune thyroiditis. The thyroid-specific gene currently showing the association with HT (and also Graves' disease) is the gene for thyroglobulin (Tg). The VDR gene is another HT predisposing gene, common for other organ-specific autoimmune diseases such as type-I diabetes or Addison's disease. Furthermore, cytokine genes such as IFN-γ, IL-4, or TGF-β indicate the association with the development and severity of HT. A complex interaction between genetic and non-genetic factors results in enhanced thyroid antigen presentation and reduced immune tolerance leading to predominantly Th1-type autoimmunity, thyroid destruction, and clinical disease. The exact mechanisms of initiation and progression of HT are yet to be clarified. This chapter explores the pathogenesis of Hashimoto's disease.