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首页> 外文期刊>Biological Trace Element Research >Dynamic Changes of CD4+CD25+ Regulatory T Cells in NOD.H-2h4 Mice with Iodine-Induced Autoimmune Thyroiditis
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Dynamic Changes of CD4+CD25+ Regulatory T Cells in NOD.H-2h4 Mice with Iodine-Induced Autoimmune Thyroiditis

机译:碘诱导的自身免疫性甲状腺炎NOD.H-2 h4 小鼠CD4 + CD25 + 调节性T细胞的动态变化

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摘要

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-2h4 mice with iodine-induced autoimmune thyroiditis (AIT), and explore potential immune mechanism of AIT induced by iodine. NOD.H-2h4 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.
机译:碘是甲状腺激素合成和代谢必不可少的微量元素,摄入量少或高均可导致甲状腺疾病,但碘与甲状腺自身免疫相互作用的致病机制尚不清楚。我们研究了由碘诱导的自身免疫性甲状腺炎(AIT)引起的NOD.H-2 h4 小鼠中CD4 + CD25 + 调节性T细胞的动态变化),并探讨碘诱导的AIT的潜在免疫机制。将NOD.H-2 h4 小鼠随机分为两组,分别接受白开水或含0.005%碘化钠的水。补充碘后八周,与对照组相比,含碘组的甲状腺炎发生率,甲状腺相对重量和血清甲状腺球蛋白抗体滴度显着增加(p <0.05)。与对照组相比,AIT小鼠的脾细胞中CD4 + CD25 + Foxp3 + T细胞更少,Foxp3 mRNA表达降低(p <0.01) ,并在甲状腺炎的发展过程中保持相对较低的水平。随着碘处理的扩展,上述变化逐渐加重。这些数据表明,CD4 + CD25 + 调节性T细胞可能参与了碘诱导的AIT的发病和发展。

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