Research on the Role of Th17Treg Cells and Their Factors in Graves' Disease with Different Iodine Nutritional Status

Abstract

Introduction: At present, studies on the role of iodine nutrition in thyroid function stratification, antibody titer, Th17/Treg cells and related factors in the pathogenesis of GD have not been carried out. Objective: The acritical aims to investigate the correlation between thyroid function and autoantibody titers of Graves' disease (GD) patients with different iodine nutritional status with Th17/Treg cells, their cytokines and transcription factors, and the role of related factors in the pathogenesis of GD. Method: The levels of serum thyroid hormone, autoantibodies and urine iodine in 100 GD patients and 60 healthy subjects are detected by electrochemiluminescence instrument and iodine-catalyzed arsenic-cerium method, respectively. The ratio of Th17 cells to Treg cells and Th17/Treg ratio in peripheral blood mononuclear cells (PBMC) are detected by immunofluorescence-labeled monoclonal antibodies and flow cytometry. Real-time fluorescence quantitative PCR is used to detect the expression levels of retinoic acid-related orphan receptor (ROR-γt) and fork head/wing-shaped spiral transcription factor 3 (Foxp3) mRNA, and the serum IL-17 and TGF-β levels are detected by ELISA. Result: As a result, the proportion of Th17 cells, serum IL-17 and ROR-γt in PBMC of GD patients with different iodine nutritional status significantly increase, while the proportion of Treg cells, the expression of Foxp3mRNA and serum TGF-β significantly decrease. The ratio of Th17/Treg cells in GD patients is significantly positively correlated with the titers of TPOAb and TgAb, and the titers of TPOAb and TgAb antibodies are significantly correlated with Th17/Treg, IL-17 and ROR-γt. Conclusion: In conclusion, thyroid hormones, autoantibodies, Th17, Treg cell ratios and dysfunctions as well as corresponding cytokines and transcription factors in GD patients with different iodine nutritional status participate in the development of GD.