[Current views on the etiopathogenesis of autoimmune thyroiditis (Hashimoto's disease)]

Autoimmune thyroiditis (Hashimoto's disease) is the most common type of inflammation of the thyroid gland. Although its etiopathogenesis is still unclear, it is defined as a polygenic disorder developing as the result of complex reactions between genetic and environmental factors. These factors lead to the breakdown of natural resistance to self-antigens and the development of auto-reactive lymphocytes and immunoglobulins. Environmental factors which play an important role in the development of autoimmune thyroiditis include iodine excess, interferon alpha and bacterial and viral infections. There are some genes whose polymorphisms have been confirmed as etiologic factors associated with the development of autoimmune thyroiditis. These are as follows: some variants of the HLA genes, PTPN and Tg genes and genes encoding proinflammatory cytokines such as: IFNgamma, TGFbeta, IL6 and IL4. Hitherto there has been no clear confirmation of the participation of the following genes polymorphisms in the development of autoimmune thyroiditis: IL, IL10, IL2beta, IL1R, IL4R, IL23R.