REVIEW article
Front. Immunol.
Sec. Mucosal Immunity
Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1668173
This article is part of the Research TopicInnovations in targeting intestinal immunity for chronic inflammatory disordersView all 5 articles
The AhR/IL-22 Axis in Chronic Gut Inflammation: Unraveling Mechanisms and Therapeutic Prospects
Provisionally accepted
- First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, China
Select one of your emails
You have multiple emails registered with Frontiers:
Notify me on publication
Please enter your email address:
If you already have an account, please login
You don't have a Frontiers account ? You can register here
Chronic inflammatory bowel diseases, including Crohn's disease (CD), ulcerative colitis (UC), and post-infectious irritable bowel syndrome (PI-IBS), are characterized by immune-mediated intestinal inflammation and epithelial barrier dysfunction. Research indicates that the aryl hydrocarbon receptor (AhR)/interleukin-22 (IL-22) pathway is critical for intestinal homeostasis. This pathway can be activated by ligands from dietary and microbial sources (such as tryptophan metabolites), and AhR signaling in immune cells (particularly type 3 innate lymphoid cells (ILC3s) and T cells) is the primary driver of IL-22 production. IL-22 protects the intestinal barrier and regulates inflammatory responses by promoting epithelial repair, enhancing mucus and antimicrobial defenses, and strengthening tight junctions. Dysregulation of this pathway plays a key role in the pathogenesis of chronic intestinal inflammation, leading to exacerbated inflammatory processes and mucosal damage. Given its central role in barrier defense and repair, targeting the AhR/IL-22 pathway has emerged as a novel therapeutic direction for restoring intestinal homeostasis. This review summarizes the mechanisms of action of this pathway in chronic intestinal inflammation and explores its potential as a novel therapeutic target.
Keywords: the AhR/IL-22 pathway, chronic intestinal inflammation, Immuneresponse, AhR, IL-22
Received: 17 Jul 2025; Accepted: 29 Aug 2025.
Copyright: © 2025 Kang, Chen, Wang and Chen. 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: Zheng Chen, First Affiliated Hospital, Zhejiang Chinese Medical University, Hangzhou, China
Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.