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硒在小鼠实验性自身免疫性甲状腺炎中调节T细胞分化。

Selenium regulates T cell differentiation in experimental autoimmune thyroiditis in mice.

作者信息

Wang Wei, Jiang Qi-Lan, Xu Qin, Zeng Yang, Jiang Rui, Jiang Jun

机构信息

Department of General Surgery/Thyroid Surgery, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China; Department of Thyroid, Head, Neck and Maxillofacial Surgery, Third Hospital of Mianyang & Sichuan Mental Health Center, Mianyang, Sichuan, China.

Department of Clinical Nutrition, Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan, China.

出版信息

Int Immunopharmacol. 2023 Nov;124(Pt B):110993. doi: 10.1016/j.intimp.2023.110993. Epub 2023 Sep 28.

DOI:10.1016/j.intimp.2023.110993
PMID:37776772
Abstract

Selenium (Se) is an essential trace element that plays an important role in thyroid physiology. Se supplementation can reduce levels of autoimmune thyroid antibodies, which may be beneficial in Hashimoto's thyroiditis (HT). However, the long-term benefits of Se supplementation for HT patients are controversial and there is no clear clinical evidence to support it, so further basic and clinical research is needed. The effect of Se on immune cells, especially T cells, in autoimmune thyroiditis (AIT) has not been elucidated. Here, we replicated a mouse model of experimental autoimmune thyroiditis (EAT) on a high-iodine diet and treated it with Se supplementation. At week 8 of the experiment, Se supplementation reduced the destruction of thyroid follicles and the infiltration rate of lymphocytes in EAT mice, and reversed the disturbance of peripheral blood thyroxine and thyroid autoantibody levels. Further examination revealed that Se had broad effects on T-cell subsets. Its effects include reducing the production of pro-inflammatory cytokines by Th1 cells, inhibiting the differentiation and production of cytokines by Th2 and Th17 cells, and upregulating the differentiation and production of cytokines by Treg cells. These changes help alleviate thyroid follicle damage during EAT. In conclusion, selenium supplementation has the potential to improve the prognosis of AIT by altering the subset differentiation and/or function of CD4+ T cells.

摘要

硒(Se)是一种必需的微量元素,在甲状腺生理过程中发挥着重要作用。补充硒可以降低自身免疫性甲状腺抗体水平,这可能对桥本甲状腺炎(HT)有益。然而,补充硒对HT患者的长期益处存在争议,且尚无明确的临床证据支持,因此需要进一步的基础和临床研究。硒在自身免疫性甲状腺炎(AIT)中对免疫细胞,尤其是T细胞的作用尚未阐明。在此,我们在高碘饮食条件下复制了实验性自身免疫性甲状腺炎(EAT)小鼠模型,并给予补充硒进行治疗。在实验第8周时,补充硒减少了EAT小鼠甲状腺滤泡的破坏和淋巴细胞浸润率,并逆转了外周血甲状腺素和甲状腺自身抗体水平的紊乱。进一步检查发现,硒对T细胞亚群有广泛影响。其作用包括减少Th1细胞促炎细胞因子的产生,抑制Th2和Th17细胞细胞因子的分化和产生,以及上调Treg细胞细胞因子的分化和产生。这些变化有助于减轻EAT期间的甲状腺滤泡损伤。总之,补充硒有可能通过改变CD4+ T细胞亚群的分化和/或功能来改善AIT的预后。

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