ABSTRACT
The thyroid gland is the target of two main organ-specific autoimmune disorders with opposite clinical outcomes in human: Hashimoto’s thyroiditis (HT) can result in hypothyroidism, and Graves’ disease in hyperthyroidism. Whereas numerous models of HT have been developed in various species, including mammals and birds, few models of Graves’ disease have been reported. Spontaneous as well as experimentally-induced autoimmune thyroiditis have largely contributed to our understanding of the mechanisms involved in HT. One general feature of autoimmune diseases, including thyroid autoimmune disorders, is their Major Histocompatibility Complex (MHC)-linked susceptibility (1). Moreover, autoimmune disorders often exhibit higher incidence in females than in males. Autoimmune processes play an important role in thyroid diseases and during the last ten years, knowledge of their mechanism greatly improved, allowing, at least in experimental models, better targeted and more specific treatments with fewer deleterious secondary effects.
