[ Etiopathogenesis of autoimmune thyroiditis]

Human autoimmune thyroid diseases include both autoimmune hypothyroidism (thyroiditis) and autoimmune hyperthyroidism (Graves' disease). Either of the two feature profuse thyroidal infiltrates of CD4+ and CD8+ T-cells and a biased intrathyroidal T-cell-receptor repertoire. Despite strong epidemiologic evidence in favor of a genetic component in the etiology of autoimmune thyroiditis, few hereditary risk factors have been consistently identified, which include a well-characterized series of HLA genes. These may account for the progression from a harmless autoimmune response characterized solely by production of autoantibodies to thyroglobulin to pathogenic autoimmunity where injury occurs to the thyroid cells. We hereafter summarize the role of inherited risk factors along with that of environmental risk factors. It was suggested that iodine increase the autoantigenic potency of thyroglobulin, a major pathogenic antigen in the induction of autoimmune thyroiditis. The clinical entities included together as autoimmune thyroiditis is shortly reviewed, along with the presentation of the common pathogenetic pathways. Unique features of each member of the group are further emphasized.