This review uncovers immune-fibrotic interactions in pulmonary fibrosis, suggesting new therapeutic strategies for treatment.
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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Kang et al. (2026) studied this question.
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