| Literature DB >> 20820943 |
Haibo Xue1, Weiwei Wang, Zhongyan Shan, Yuanbin Li, Yushu Li, Xiaochun Teng, Yun Gao, Chenling Fan, Weiping Teng.
Abstract
Iodine is an essential trace element for thyroid hormone synthesis and metabolism, either low or high intake may lead to thyroid disease, but the pathogenetic mechanisms by which iodine interacts with the thyroid autoimmune are poorly understood. We investigated the dynamic changes of CD4(+)CD25(+) regulatory T cells in NOD.H-2(h4) mice with iodine-induced autoimmune thyroiditis (AIT), and explore potential immune mechanism of AIT induced by iodine. NOD.H-2(h4) mice were randomly divided into two groups, and received plain water or water containing 0.005% sodium iodide. Eight weeks after iodine provision, the incidences of thyroiditis, relative weights of thyroids, and serum thyroglobulin antibody titers in the iodine-supplied groups were significantly increased compared to the control groups (p < 0.05). The AIT mice had fewer CD4(+)CD25(+)Foxp3(+) T cells and reduced Foxp3 mRNA expression in splenocytes compared with the controls (p < 0.01), and maintained relatively low levels during the development of thyroiditis. The changes described above aggravated gradually with the extension of iodine treatment. These data suggest that CD4(+)CD25(+) regulatory T cells may be involved in the pathogenesis and development of AIT induced by iodine.Entities:
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Year: 2010 PMID: 20820943 DOI: 10.1007/s12011-010-8815-x
Source DB: PubMed Journal: Biol Trace Elem Res ISSN: 0163-4984 Impact factor: 3.738