Research advance in Hashimoto thyroiditis mediated by T helper cell 17
10.3760/cma.j.cn311282-20220328-00186
- VernacularTitle:辅助性T细胞17介导桥本甲状腺炎发病机制的研究现状
- Author:
Xueqi ZHANG
1
;
Fan ZHANG
;
Weiping TENG
Author Information
1. 中国医科大学附属第一医院内分泌与代谢病科，内分泌研究所；卫生健康委员会(共建)甲状腺疾病诊治重点实验室，沈阳 110001
- Keywords:
Hashimoto thyroiditis;
T helper cell 17;
Regulatory T cell;
Immune
- From:
Chinese Journal of Endocrinology and Metabolism
2022;38(11):1001-1005
- CountryChina
- Language:Chinese
-
Abstract:
Hashimoto thyroiditis(HT) is a classic autoimmune thyroiditis (AIT), characterized by diffuse lymphocytic infiltration, destruction of thyroid structure, and positive autoantibodies. The pathogenesis of HT is complex and related to genetic susceptibility, immune system disorders, and environmental factors. The imbalance of T helper cell 1 (Th1)/ T helper cell 2 (Th2) is traditionally believed to be the main mechanism of HT. However, recent studies have shown that T helper cell 17 (Th17) plays an important role in the occurrence and development of HT through non-coding RNA regulation, autophagy-related pathway regulation, the balance with regulatory T cell (Treg). These mechanisms can enhance the release of inflammatory factors and aggravate HT by stimulating the differentiation of Th17, the inflammatory environment of HT also further stimulates the differentiation of Th17 and amplifies the inflammatory response. The regulatory mechanisms of Th17 are complex and have not yet been fully studied. Therefore, this article reviews the related mechanism of Th17 in HT to provide insights for novel therapeutic targets.
