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REVIEW article

Front. Immunol.

Sec. T Cell Biology

This article is part of the Research TopicT Regulatory Cells: Mechanisms and Therapeutical AdvancesView all 4 articles

Metabolic Reprogramming as a Therapeutic Target for Modulating the Th17/Treg Balance in Autoimmune Diseases: A Comprehensive Review

Provisionally accepted
  • Beijing Hospital of Traditional Chinese Medicine, Capital Medical University, Beijing, China

The final, formatted version of the article will be published soon.

The dynamic balance between T helper 17 (Th17) cells and regulatory T (Treg) is the cornerstone of immune homeostasis. Disruption of this equilibrium is closely associated with various autoimmune diseases, including rheumatoid arthritis (RA), multiple sclerosis (MS), and inflammatory bowel disease (IBD). Studies have revealed that metabolic reprogramming, mediated by key metabolic enzymes (including mTOR, HIF-1α, and AMPK) and pathways (such as glycolysis and lipid metabolism), acts as a major regulator of Th17/Treg differentiation and function owing to their distinct metabolic profiles. Metabolic dysregulation may exacerbate immune imbalance by altering the cellular differentiation trajectories and functional states. Although targeting metabolic pathways shows therapeutic promise, current intervention strategies face challenges in terms of specificity and safety. This review systematically combs the mechanisms by which metabolic reprogramming influences the differentiation and function of Th17/Treg cells, as well as the metabolic changes in immune cells of inflammation-related autoimmune diseases. It outlines the progress of the latest metabolism-targeted strategies and focuses on discussing the challenges and prospects regarding the specificity and safety of metabolic interventions.

Keywords: Immunometabolism, Th17/Treg balance, Autoimmune Diseases, Therapeutic target, mTOR

Received: 18 Aug 2025; Accepted: 17 Nov 2025.

Copyright: © 2025 Hu, Zhao, Dai, Wu, Tang, Zhang, Jiang, Rui and Liu. 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: Baoli Liu, liubaoli@bjzhongyi.com

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