The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets

Pulmonary fibrosis is the converging pathological outcome of chronic inflammatory lung diseases with diverse etiologies. Sustained inflammation disrupts immune cell homeostasis, driving aberrant activation and differentiation of myofibroblasts and leading to excessive extracellular matrix deposition within the lung interstitium. Emerging evidence indicates that immune dysregulation contributes to myofibroblast activation, and that immunomodulatory therapies may reverse fibrotic progression across diverse disease models. In this Review, we dissect the mechanisms by which immune dysregulation promotes fibrosis in distinct pathological contexts, highlighting the heterogeneity of immune-fibrotic interactions. We further discuss emerging targets with potential for precision intervention, aiming to inform the development of adjunctive and personalized therapeutic strategies.

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Publication Details

Journal
Frontiers in Immunology
Published
2026-03-11
DOI
https://doi.org/10.3389/fimmu.2026.1770516
Primary Topic
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
Type
article
Field-Weighted Citation Impact
0.00

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article

The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets

Ling-Zhen Jiang, L. Wang, Yanan Xiao, Yi-Fei Fu et al.
Frontiers in Immunology
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
article

The immune dysregulation of fibrosis: insights into immune-fibrotic crosstalk and potential therapeutic targets

Ling-Zhen Jiang, L. Wang, Yanan Xiao, Yi-Fei Fu, Zhi-Tong Zuo, Xie-Lin Yan, Hao Wu, Zhen-Zhu Zhang, Jun-Jie Wu, Feng-Lai Yuan, Hua-Xin Kang
article en

Abstract

Pulmonary fibrosis is the converging pathological outcome of chronic inflammatory lung diseases with diverse etiologies. Sustained inflammation disrupts immune cell homeostasis, driving aberrant activation and differentiation of myofibroblasts and leading to excessive extracellular matrix deposition within the lung interstitium. Emerging evidence indicates that immune dysregulation contributes to myofibroblast activation, and that immunomodulatory therapies may reverse fibrotic progression across diverse disease models. In this Review, we dissect the mechanisms by which immune dysregulation promotes fibrosis in distinct pathological contexts, highlighting the heterogeneity of immune-fibrotic interactions. We further discuss emerging targets with potential for precision intervention, aiming to inform the development of adjunctive and personalized therapeutic strategies.

Frontiers in ImmunologyVol. 17
Jiangnan University (CN), Shanghai Jiao Tong University (CN), Tongren Hospital (CN), Wuxi Fourth People's Hospital (CN)
Government of Jiangsu Province
Good health and well-being
Openalex Percentile: Top 26%
Interstitial Lung Diseases and Idiopathic Pulmonary Fibrosis
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