Department of Endocrinology and Metabolism, Institute of Endocrinology, The First Affiliated Hospital, China Medical University, Liaoning Provincial Key Laboratory of Endocrine Diseases, Shenyang 110001, P. R. China.
J Reprod Immunol. 2018 Apr;126:23-31. doi: 10.1016/j.jri.2018.02.001. Epub 2018 Feb 7.
Previous studies have reported a preponderance of autoimmune thyroiditis (AIT) in females, but the detailed mechanisms have not been elucidated. In this study, we explored the effects of oestrogen on experimental AIT (EAT) and its potential mechanisms in an ovariectomised mouse model through the supplementation of high (equivalent to the level during pregnancy) or low (equivalent to the level at the oestrus stage) doses of oestradiol (E2). We found that EAT incidence, the intrathyroidal inflammatory score, serum anti-thyroglobulin IgG2b levels, splenic mRNA expression of Th1- and Th17-specific transcription factors and typical cytokines and the proportion of IL-12-producing dendritic cells were significantly increased in EAT mice treated with low-dose E2 compared with those in the control group. However, they were not changed when administered with high-dose E2. These findings indicate that low physiological levels of E2 can stimulate the occurrence and development of EAT through the up-regulation of Th1/Th17 responses.
先前的研究报告表明，女性自身免疫性甲状腺炎（AIT）更为常见，但详细的机制尚未阐明。在这项研究中，我们通过补充高（相当于妊娠水平）或低（相当于发情期水平）剂量的雌二醇（E2），在去卵巢小鼠模型中探索了雌激素对实验性自身免疫性甲状腺炎（EAT）的影响及其潜在机制。我们发现，与对照组相比，低剂量 E2 处理的 EAT 小鼠的 EAT 发生率、甲状腺内炎症评分、血清抗甲状腺球蛋白 IgG2b 水平、脾组织中 Th1 和 Th17 特异性转录因子和典型细胞因子的 mRNA 表达以及产生 IL-12 的树突状细胞的比例均显著增加。然而，当给予高剂量 E2 时，这些变化并未发生。这些发现表明，低生理水平的 E2 可以通过上调 Th1/Th17 反应来刺激 EAT 的发生和发展。
