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Background <p>Radiation induced pulmonary fibrosis (RIPF) is a life threatening and frequent complication that can occur after radiotherapy to thoracic cancers, and has a complicated pathogenesis and few treatment options. Recent data suggest that immune cells are the centerpiece of this mechanism, and constitute a complex system of regulation.</p> Objective <p>This review systematically summarizes the dynamic roles and molecular mechanisms of key immune cells in RIPF initiation and progression, and reviews current advances in targeted immunotherapies.</p> Methods <p>A comprehensive literature search was conducted in PubMed and Web of Science for studies on immune regulation and therapeutic strategies in RIPF.</p> Results <p>RIPF exhibits profound spatiotemporal heterogeneity, with immune cell subsets evolving dynamically from inflammation to fibrosis. Macrophages transcend the M1/M2 dichotomy, encompassing specialized subsets. Neutrophils promote fibrosis via NETosis and STAT3/NLRP3 pathways, while eosinophils switch from protective to pathogenic phenotypes. Beyond Th1/Th2 imbalance, Tregs and Th17 cells critically contribute to fibrosis. Emerging targeted strategies—including nanomaterials, natural compounds, and specific inhibitors—have shown promising preclinical results.</p> Conclusion <p>Understanding the spatiotemporally specific functions of immune cells is crucial for developing precision immunotherapies. Future research should focus on biomarker-guided combination strategies to transform RIPF into a preventable and manageable condition.</p>

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Multifaceted regulation of immune cells in radiation-induced pulmonary fibrosis: from mechanistic insights to targeted therapies

  • 期刊论文

  • 发表日期：

    2026年4月2日

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  • Li Shen,
  • Wanrong Zhang,
  • Yonghao Yang,
  • Zhiqiang Du,
  • Shiyan Fu,
  • Feng Huang,
  • Xiaoyu Yang,
  • Juan Li,
  • Yonghong Ran,
  • Yuhui Hao

摘要

Background

Radiation induced pulmonary fibrosis (RIPF) is a life threatening and frequent complication that can occur after radiotherapy to thoracic cancers, and has a complicated pathogenesis and few treatment options. Recent data suggest that immune cells are the centerpiece of this mechanism, and constitute a complex system of regulation.

Objective

This review systematically summarizes the dynamic roles and molecular mechanisms of key immune cells in RIPF initiation and progression, and reviews current advances in targeted immunotherapies.

Methods

A comprehensive literature search was conducted in PubMed and Web of Science for studies on immune regulation and therapeutic strategies in RIPF.

Results

RIPF exhibits profound spatiotemporal heterogeneity, with immune cell subsets evolving dynamically from inflammation to fibrosis. Macrophages transcend the M1/M2 dichotomy, encompassing specialized subsets. Neutrophils promote fibrosis via NETosis and STAT3/NLRP3 pathways, while eosinophils switch from protective to pathogenic phenotypes. Beyond Th1/Th2 imbalance, Tregs and Th17 cells critically contribute to fibrosis. Emerging targeted strategies—including nanomaterials, natural compounds, and specific inhibitors—have shown promising preclinical results.

Conclusion

Understanding the spatiotemporally specific functions of immune cells is crucial for developing precision immunotherapies. Future research should focus on biomarker-guided combination strategies to transform RIPF into a preventable and manageable condition.