Selenium upregulates CD4+CD25+ regulatory T cells in iodine-induced autoimmune thyroiditis model of NOD.H-2h4 mice

Selenium (Se) is required for thyroid hormone synthesis and metabolism. Se treatment reduces serum thyroid-specific antibody titers in patients with autoimmune thyroiditis (A IT), but the exact mechanism is not clear. We investigated the effects of Se treatment on CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) in a iodine-induced autoimmune thyroiditis model. NOD.H-2(h4) mice were randomly divided into control, AIT untreated, and AIT with Se treatment groups. Mice were fed with 0.005% sodium iodine (NaI) water for 8 weeks to induce AIT. Se-treated mice received 0.3 mg/L sodium selenite in drinking water. The AIT mice had fewer Treg cells and reduced Foxp3 mRNA expression in splenocytes compared with the controls (p<0.01). The percentage of Treg cells and expression of Foxp3 mRNA were increased by Se treatment (as compared with untreated AIT mice, p<0.05). Mice that received Se supplementation also had lower serum thyroglobulin antibody (TgAb) titers and reduced lymphocytic infiltration in thyroids than untreated AIT mice. These data suggest that CD4(+)CD25(+) T cells play an important role in the development of ALT. Se supplementation may restore normal levels of CD4(+)CD25(+) T cells by upregulating the expression of Foxp3 mRNA in mice with AIT.