REVIEW article
Front. Immunol.
Sec. Inflammation
This article is part of the Research TopicCytokines in inflammatory, infectious and noninfectious diseasesView all 8 articles
Interleukin-37 in respiratory diseases: molecular mechanisms and immune modulation
Provisionally accepted
- Second Hospital of Hebei Medical University, Shijiazhuang, 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
Interleukin-37 (IL-37) is a potent anti-inflammatory cytokine that plays a crucial protective role in cancer, autoimmune diseases, and inflammatory diseases though its unique dual intracellular and extracellular action pathways. This review highlights the significance of IL-37 in common respiratory diseases. Specifically, IL-37 can alleviate asthma by inhibiting Th2/Th17 immune responses, inhibiting the release of epithelial-derived alarmins (TSLP and IL-33), and attenuating airway remodeling. In pulmonary infections, IL-37 modulates host responses by mitigating virus-induced hyperinflammation and inhibiting viral replication, as observed in COVID-19 and influenza, while also regulating immunopathology in Mycobacterium tuberculosis and fungal infections. Moreover, in non-small cell lung cancer (NSCLC), IL-37 directly suppresses tumor proliferation and migration, and restrains tumor progression through immunomodulation and angiogenesis regulation. In pulmonary fibrosis, IL-37 reduces collagen deposition and promotes autophagy, thereby counteracting interstitial fibrosis. Collectively, these findings demonstrate that IL-37 serves as a crucial immunomodulator in respiratory diseases, and targeting IL-37 offers novel insights and strategic opportunities for clinical intervention. This review systematically summarizes the molecular mechanisms of IL-37 and discusses its clinical therapeutic potential.
Keywords: Interleukin-37, Asthma, pulmonary infection, NSCLC, pulmonary interstitialfibrosis
Received: 29 Jul 2025; Accepted: 24 Oct 2025.
Copyright: © 2025 Cao, He, Chen, Xu, Wei, Yan and Song. 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: Beibei Song, 15830996001@163.com
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.