Selenium is an essential trace element in human. Recent studies of selenium (Se) supplementation on the effect of Hashimoto thyroiditis (HT) have been reported, but the exact benefit is unclear as well as the underlying immunologic mechanism. We aimed to evaluate the clinical effect of selenium (Se) treatment in HT patients, and explore the potential mechanism against thyroid autoimmunity. A prospective, randomized-controlled study was performed in HT patients assigned to two groups. Se-treated group (n=43) received Se-yeast for 6 months, while no treatment in control group (n=47). The primary outcome is the changement of thyroid antibody (TPOAb or TGAb). Secondly, thyroid function, urinary iodine (UI), Se, Glutathione peroxidase3 (GPx3) and Selenoprotein P1 (SePP1) levels were measured during the treatment. Meanwhile, regulatory T cells (Tregs) and their subsets activated Tregs (aTregs), resting Tregs (rTregs) and secreting Tregs (sTregs), as well as Helios and PD-1 expression on these cells were also detected. The results showed that Se supplementation significantly decreased thyroid peroxidase antibody (TPOAb), thyroglobulin antibody (TGAb), and thyroid stimulating hormone (TSH) levels, accompanied with the increased Se, GPx3 and SePP1, compared with control group. Subgroup analysis revealed that subclinical HT may benefit more from this treatment in the decrease of TSH levels by interaction test. Moreover, the percentage of aTregs, Helios/Tregs, and Helios/aTregs were significantly higher in Se group than control. In conclusion, Se supplementation may have a beneficial effect on thyroid autoantibodies and thyroid function by increasing the antioxidant activity and upregulating the activated Treg cells.
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