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Analysis of polymorphisms CT60 of CTLA4 gene and -1623A/G in the promoter region of the thyroglobulin gene in patients with Graves' disease

Grant number: 12/23213-7
Support Opportunities:Regular Research Grants
Duration: June 01, 2013 - May 31, 2015
Field of knowledge:Biological Sciences - Genetics - Human and Medical Genetics
Principal Investigator:Suemi Marui
Grantee:Suemi Marui
Host Institution: Faculdade de Medicina (FM). Universidade de São Paulo (USP). São Paulo , SP, Brazil


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 thyroidantigens, such as thyroperoxidase, thyroglobulin, TSH receptor, sodium-iodine symporter. Genetic and epigenetic factors have roles in triggering GD, like C TLA4 and TG genes, as well as substances that induce thyroid autoimmunity (amiodarone, lithium, interferon and iodine). Recently it was demonstrated that avariation 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, whichinteracts 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), C TLA4 also seems to predispose to DG. Our group studied the association of C TLA4polymorphisms in children and adolescents with AITD (GD and Hashimoto's thyroiditis) (FAPESP 09/17327-7) and found the association with the C T60 polymorphism. Our group also investigated the incidence ofAITD in patients with hepatitis C virus and treated with IFNa, and it was not possible to determine anassociation with C TLA4 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 polymorphismC T60 of C TLA4 in patients with Graves' disease. (AU)

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