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Indexed/Abstracted in: EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 1,118
Online ISSN 1827-1634
Yeganeh ESHAGHKHANI 1, Mohammad H. SANATI 1, Manouchehr NAKHJAVANI 2, Reza SAFARI 2, Alireza KHAJAVI 3, Mitra ATAEI 1, Zohreh JADALI 4
1 Clinical Genetics Department, National Institute of Genetic Engineering and Biotechnology, Tehran, Iran; 2 Endocrinology and Metabolism Research Center (EMRC), Vali-Asr Hospital, School of Medicine, Tehran University of Medical Sciences , Tehran, Iran; 3 Department of Biostatics and Epidemiology School of Public Health Tehran University of Medical Sciences, Tehran, Iran; 4 Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
BACKGROUND AND METHODS: Graves’ disease (GD) is a common autoimmune disorder that is primarily driven by malfunction of T lymphocytes, which influences the production of antibodies reacting with cellular and tissue components of the thyroid gland. The aim of this study was to determine the level of mRNA expression for the genes encoding T-bet and GATA3, as the master regulators of the T helper (Th)1 and Th2 differentiation, respectively together with Th1 (IFN-γ) and Th2(IL-4) cytokine mRNA expression. Relative quantification of T-bet, GATA3, IFN-γ and IL-4 transcripts in peripheral blood mononuclear cell (PBMCs) was conducted by real-time reverse transcriptase PCR (RT-PCR). Serum levels of IFN-γ and IL-4 were also determined by Enzyme-linked immunosorbent assay (ELISA). In comparison with the normal group, T-bet and IFN-γ mRNA expression levels were significantly up-regulated in the GD patients, while GATA3 and IL-4 mRNA expression levels were downregulated. In addition, a marked decrease in plasma IL-4 levels was observed in the GD group. IFN-γ levels were also higher in patients in comparison to the controls. Furthermore, a clear correlation between increased IFN-γ mRNA expression and IFN-γ (P<0.05) was revealed. These results indicate that a Th1/Th2 imbalance exists in GD, and it may be implicated in the pathogenesis of disease.