{"title":"Research progress on estrogen and estrogen receptors in the occurrence and progression of autoimmune thyroid diseases","authors":"Jiewen Xie , Jie Wang , Xuejiao Cui","doi":"10.1016/j.autrev.2025.103803","DOIUrl":null,"url":null,"abstract":"<div><div>Autoimmune thyroid disease (AITD) is a category of disease related to sex differences, with a significantly higher incidence in women than in men. In addition to X chromosome inactivation abnormalities, Estrogen and estrogen receptors may lead to the sex differences in AITD. Estrogen, estrogen receptors and estrogen receptor-mediated signaling pathways can affect the number and function of immune cells and the function of the thyroid to promote the development of AITD. This article describes the role of estrogen in regulating the composition ratio and the function of immune cells and the role of estrogen in promoting thyroid cell proliferation and thyroxine-binding protein and thyroid antibody production; the role of estrogen in stimulating the hypothalamus-pituitary–thyroid gland axis; and the role of estrogen and the estrogen receptor in the progression of AITD. These roles offer a new perspective for understanding the pathological mechanism of AITD and provide new targets for future therapeutic strategies.</div></div>","PeriodicalId":8664,"journal":{"name":"Autoimmunity reviews","volume":"24 6","pages":"Article 103803"},"PeriodicalIF":9.2000,"publicationDate":"2025-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Autoimmunity reviews","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1568997225000631","RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Autoimmune thyroid disease (AITD) is a category of disease related to sex differences, with a significantly higher incidence in women than in men. In addition to X chromosome inactivation abnormalities, Estrogen and estrogen receptors may lead to the sex differences in AITD. Estrogen, estrogen receptors and estrogen receptor-mediated signaling pathways can affect the number and function of immune cells and the function of the thyroid to promote the development of AITD. This article describes the role of estrogen in regulating the composition ratio and the function of immune cells and the role of estrogen in promoting thyroid cell proliferation and thyroxine-binding protein and thyroid antibody production; the role of estrogen in stimulating the hypothalamus-pituitary–thyroid gland axis; and the role of estrogen and the estrogen receptor in the progression of AITD. These roles offer a new perspective for understanding the pathological mechanism of AITD and provide new targets for future therapeutic strategies.
期刊介绍：
Autoimmunity Reviews is a publication that features up-to-date, structured reviews on various topics in the field of autoimmunity. These reviews are written by renowned experts and include demonstrative illustrations and tables. Each article will have a clear "take-home" message for readers.
The selection of articles is primarily done by the Editors-in-Chief, based on recommendations from the international Editorial Board. The topics covered in the articles span all areas of autoimmunology, aiming to bridge the gap between basic and clinical sciences.
In terms of content, the contributions in basic sciences delve into the pathophysiology and mechanisms of autoimmune disorders, as well as genomics and proteomics. On the other hand, clinical contributions focus on diseases related to autoimmunity, novel therapies, and clinical associations.
Autoimmunity Reviews is internationally recognized, and its articles are indexed and abstracted in prestigious databases such as PubMed/Medline, Science Citation Index Expanded, Biosciences Information Services, and Chemical Abstracts.
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