RAR相关孤儿受体γ
甲状腺球蛋白
自身免疫性甲状腺炎
医学
免疫学
甲状腺过氧化物酶
自身抗体
调节性T细胞
FOXP3型
甲状腺炎
发病机制
内分泌学
T细胞
内科学
抗体
免疫系统
甲状腺
白细胞介素2受体
作者
Hui Zhu,Shumin Mu,Shiyin Liu,Cui Yang,Jianyu Ren,Enquan Yang,Lining Wang,X. Cui,Ailing Ren
出处
期刊:Endocrine, metabolic & immune disorders
[Bentham Science]
日期:2024-02-03
卷期号:24 (10): 1186-1196
被引量:1
标识
DOI:10.2174/0118715303256311231122094516
摘要
Background: Experimental autoimmune thyroiditis (EAT) is a widely used animal model to study the pathogenesis and treatment of autoimmune thyroid diseases. Yiqi Jiedu Xiaoying Decoction (YJXD) is a traditional Chinese medicine formula with potential immunomodulatory effects. In this study, we investigated the therapeutic effects of YJXD on EAT in rats and explored its underlying mechanisms. Methods: Female Wistar rats were induced to develop EAT by immunization with thyroglobulin (Tg) and taken sodium iodide water (0.05%) and then treated with YJXD or sodium selenite. HE staining was used to observe the pathological changes of thyroid tissue in EAT rats. Th17 and Treg cell frequencies were analyzed by flow cytometry, and the expression levels of Th17- and Treg-related cytokines and thyroid autoantibody were determined by enzyme-linked immunosorbent assay (ELISA). The expression of Th17- and Treg-related transcriptional factors was detected by real-time polymerase chain reaction (RT-PCR) and Immunohistochemistry (IHC). Results: Our results demonstrated that treatment with YJXD significantly attenuated the severity of EAT, as evidenced by reduced thyroid gland inflammatory infiltration and decreased serum thyroglobulin autoantibody levels. Importantly, YJXD treatment effectively modulated the Th17/Treg cell balance by suppressing Th17 cell differentiation and promoting Treg cell expansion. Moreover, YJXD was also found to regulate the expression levels of Th17- and Treg-related cytokines and transcriptional factors, further supporting its immunomodulatory effects in EAT. Conclusion: YJXD exerted therapeutic effects on EAT by regulating the Th17/Treg cell balance, modulating the production of Th17- and Treg-related cytokines and the expression of transcriptional factors.
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