Journal
ENDOCRINE JOURNAL
Volume 57, Issue 7, Pages 595-601Publisher
JAPAN ENDOCRINE SOC
DOI: 10.1507/endocrj.K10E-063
Keywords
Selenium; NOD.H-2(h4) mice; Autoimmune thyroiditis; Regulatory T cells
Categories
Funding
- National High Technology Research and Development Program of China [2007AA02Z4Z1]
- Ministry of Education [20070159007]
- Key Laboratory Project of Liaoning Province [2008S225]
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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.
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