دورية أكاديمية

Leptin receptor antagonist attenuates experimental autoimmune thyroiditis in mice by regulating Treg/Th17 cell differentiation

التفاصيل البيبلوغرافية
العنوان: Leptin receptor antagonist attenuates experimental autoimmune thyroiditis in mice by regulating Treg/Th17 cell differentiation
المؤلفون: Wei Wang, Bo-Tao Zhang, Qi-Lan Jiang, Han-Qing Zhao, Qin Xu, Yang Zeng, Jia-Ying Xu, Jun Jiang
المصدر: Frontiers in Endocrinology, Vol 13 (2022)
بيانات النشر: Frontiers Media S.A., 2022.
سنة النشر: 2022
المجموعة: LCC:Diseases of the endocrine glands. Clinical endocrinology
مصطلحات موضوعية: leptin, experimental autoimmune thyroiditis (EAT), JAK2/STAT3 pathway, leptin receptor antagonist, NOD/ShiLtJ mouse, Diseases of the endocrine glands. Clinical endocrinology, RC648-665
الوصف: Leptin has been found to be involved in the development and progression of many autoimmune diseases. As an organ-specific autoimmune disease, the pathogenesis of Hashimoto’s thyroiditis has not been fully elucidated. It has been reported that serum leptin level is increased in Hashimoto’s thyroiditis, but other studies have not shown any difference. We replicated a mouse model of experimental autoimmune thyroiditis (EAT) with a high-iodine diet and found that injection of the leptin receptor antagonist Allo-aca reduced thyroid follicle destruction and inflammatory cell infiltration in EAT mice, and thyroxine and thyroid autoimmune antibody levels. Further investigation revealed that Allo-aca promotes the differentiation of Treg cells and inhibits the differentiation of Th17 cells. We believe that Allo-aca can alter the differentiation of Treg/Th17 cells by inhibiting the leptin signaling pathway, thereby alleviating thyroid injury in EAT mice. Interfering with the leptin signaling pathway may be a novel new approach to treat treating and ameliorating Hashimoto’s thyroiditis.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1664-2392
Relation: https://www.frontiersin.org/articles/10.3389/fendo.2022.1042511/full; https://doaj.org/toc/1664-2392
DOI: 10.3389/fendo.2022.1042511
URL الوصول: https://doaj.org/article/c8d40158ed964e2e93f9b2d0684dd45c
رقم الأكسشن: edsdoj.8d40158ed964e2e93f9b2d0684dd45c
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:16642392
DOI:10.3389/fendo.2022.1042511