Graves' disease (GD) is responsible for 60-80% of patients affected by hyperthyroidism. GD has autoimmune characteristics, with production of autoantibodies produced by B lymphocytes against thyroid antigens, such as thyroperoxidase, thyroglobulin, TSH receptor, sodium-iodine symporter. Genetic and epigenetic factors have roles in triggering GD, like CTLA4 and TG genes, as well as substances that induce thyroid autoimmunity (amiodarone, lithium, interferon and iodine). Recently it was demonstrated that a variation in the promoter region of TG gene (-1623A / G) changes the binding site of interferon regulatory factor-1 (IRF-1), increasing TG expression and acetylation and methylation of aminoacid in this site. Interferon-± (IFNa) is a cytokine produced by macrophages and dendritic cells in viral infections, which interacts with the TG through the IRF-1, increasing its transcription, and favoring therefore thyroid autoimmunity. Although TG gene is one of the main genetic components of autoimmune thyroid diseases (AITD), CTLA4 also seems to predispose to DG. Our group studied the association of CTLA4 polymorphisms in children and adolescents with AITD (GD and Hashimoto's thyroiditis) (FAPESP 09/17327-7) and found the association with the CT60 polymorphism. Our group also investigated the incidence of AITD in patients with hepatitis C virus and treated with IFNa, and it was not possible to determine an association with CTLA4 polymorphisms, probably due to the heterogeneity of our population. Therefore, this study aims to determine association of the new polymorphism-1623A / G in TG and polymorphism CT60 of CTLA4 in patients with Graves' disease.
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