Department of Endocrinology and Metabolism, Institute of Endocrinology, The First Affiliated Hospital, China Medical University, Shenyang, China.
Biol Trace Elem Res. 2011 Oct;143(1):292-301. doi: 10.1007/s12011-010-8815-x. Epub 2010 Sep 7.
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.
碘是甲状腺激素合成和代谢所必需的微量元素,无论是低碘还是高碘摄入都可能导致甲状腺疾病,但碘与甲状腺自身免疫相互作用的发病机制尚不清楚。我们研究了碘诱导自身免疫性甲状腺炎(AIT)中 NOD.H-2(h4)小鼠 CD4(+)CD25(+)调节性 T 细胞的动态变化,并探讨了碘诱导 AIT 的潜在免疫机制。NOD.H-2(h4)小鼠随机分为两组,分别给予普通水或含 0.005% 碘化钠的水。碘供应 8 周后,与对照组相比,碘供应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明显增加(p < 0.05)。与对照组相比,AIT 小鼠脾细胞中的 CD4(+)CD25(+)Foxp3(+)T 细胞减少,Foxp3 mRNA 表达降低(p < 0.01),并且在甲状腺炎的发展过程中保持相对较低的水平。上述变化随着碘治疗的延长而逐渐加重。这些数据表明,CD4(+)CD25(+)调节性 T 细胞可能参与了碘诱导的 AIT 的发病机制和发展。