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Decoding the Cardiac Immune Microenvironment and Fibroblast Crosstalk in Radiotherapy Combined with

Yuxi Luo1,2,3, Ying Yu1,2,3, Zhimin Zeng1,2,3

  • 1Department of Oncology, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, Jiangxi Province, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|February 20, 2026
PubMed
Summary

Radioimmunotherapy causes cardiac fibrosis via fibroblast-immune cell crosstalk, driven by IL-6. Tocilizumab (IL-6R inhibitor) shows potential to reduce this cardiotoxicity.

Keywords:
cardiac fibrosisfibroblastsimmune checkpoint inhibitorimmune microenvironmentthoracic radiotherapy

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Area of Science:

  • Cardiovascular Research
  • Immunology
  • Oncology

Background:

  • Combined radioimmunotherapy offers potent antitumor effects but poses significant cardiotoxicity risks.
  • The precise mechanisms underlying radioimmunotherapy-induced cardiotoxicity remain largely unknown.

Purpose of the Study:

  • To elucidate the mechanisms of cardiotoxicity induced by radioimmunotherapy.
  • To investigate the therapeutic potential of targeting IL-6 signaling in mitigating radioimmunotherapy-induced cardiac damage.

Main Methods:

  • Utilized preclinical models to evaluate cardiac function and fibrosis post-radioimmunotherapy.
  • Conducted single-cell RNA sequencing (scRNA-seq) and molecular analyses.
  • Employed IL-6 knockout mice and tocilizumab (an IL-6 receptor inhibitor) for targeted mechanistic studies.

Main Results:

  • Radioimmunotherapy significantly increased cardiac fibrosis and fibroblast-immune cell interactions, with IL-6 signaling predominantly from fibroblasts.
  • Elevated IL-6 levels were observed in patients undergoing thoracic radioimmunotherapy.
  • Both IL-6 knockout and tocilizumab treatment ameliorated cardiac injury, inflammation, and fibrosis.
  • Tocilizumab suppressed IL-6+ fibroblast-mediated activation of fibroblasts and CCR2+ macrophages, reducing pro-fibrotic activity.

Conclusions:

  • Fibroblast-immune cell interactions, specifically IL-6-driven fibroblast-macrophage crosstalk, are critical in radioimmunotherapy-induced cardiac fibrosis.
  • Tocilizumab presents a promising therapeutic strategy for attenuating radioimmunotherapy-related cardiotoxicity.