REVIEW article
Front. Cell. Infect. Microbiol.
Sec. Microbes and Innate Immunity
This article is part of the Research TopicInnate Reproductive Immunology and Microbial Recognition Mechanisms in Mammalian Reproductive SystemsView all articles
Thyroid-Reproductive Axis Interplay: Immunological Mechanisms and Implications for Female Reproductive Health
Provisionally accepted
- 1Hubei University of Medicine, Shiyan, China
- 2Dubai Medical College for Girls, Dubai, United Arab Emirates
- 3University of Science and Technology of China, Hefei, China
- 4King Khalid University, Abha, Saudi Arabia
- 5The University of Kansas Medical Center, Kansas City, United States
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Thyroid dysfunction is a common endocrine disease among women of childbearing age, which seriously affects reproductive health. From an immunological perspective, this in-depth analysis clarifies the complex relationship between thyroid function and female reproduction. We studied the hypothalamic-pituitary-gonadal axis regulation by thyroid hormones through direct and indirect mechanisms, including metabolic mediators such as prolactin and leptin. Recent studies have shown that inflammatory cytokines (IL-1α, IL-1β, IL-6, IFN-γ, and TNF-α) severely disrupt the production pathways of thyroid hormones, establishing an essential link between immune activation and reproductive problems. Since the placenta serves as an active immune interface affected by thyroid activity, there are significant physiological obstacles (including increased iodine clearance and elevated deiodinase activity), immunological challenges (such as altered cytokine profiles), and pathological barriers to optimal thyroid adaptation during pregnancy. This literature review indicates that thyroid problems substantially affect reproductive outcomes by altering the immune response at the maternal-fetal interface, influencing placental development, trophoblast invasion, and vascular remodeling. This review addresses a notable research deficiency through a modern perspective on thyroid dysfunction and reproductive issues, especially inflammatory cytokines related to preeclampsia. We believe that thyroid dysfunction can alter the expression of specific angiogenic factors (including sFlt-1, PlGF, and VEGF) and modify the immune cell profile at the maternal-fetal interface (particularly NK cells, macrophages, and T regulatory cells), creating a new framework for understanding and addressing thyroid-related reproductive diseases through targeted immunomodulatory strategies.
Keywords: thyroid autoimmunity, maternal-fetal interface, inflammatory cytokines, reproductive immunology, Placental development
Received: 24 Jun 2025; Accepted: 24 Oct 2025.
Copyright: © 2025 Chen, Ullah Khan, Khan, Ibrahim, Ahmad and Zhou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Safir Ullah Khan, safir@mail.ustc.edu.cn
Kun Zhou, zhoukun@taihehospital.com
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