Cao Shiwen,Jiao Yang.Progress in research on the mechanism of immune cell interaction networks in regulating radiation-induced lung injury[J].Chinese Journal of Radiological Medicine and Protection,2026,46(5):547-554
Progress in research on the mechanism of immune cell interaction networks in regulating radiation-induced lung injury
Received:July 15, 2025  
DOI:10.3760/cma.j.cn112271-20250715-00250
KeyWords:Ionizing radiation  Immune microenvironment  Intercellular interactions  Radiation pneumonitis  Radiation-induced lung fibrosis
FundProject:国家自然科学基金(82574020, 82073476, 82473565, U24A20765);国家卫生健康委核技术医学转化重点实验室开放课题(2023HYX005);四川省放射与治疗临床医学研究中心开放课题(2024ZX01);苏州市基础研究项目(SJC2023001)
Author NameAffiliation
Cao Shiwen State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China 
Jiao Yang State Key Laboratory of Radiation Medicine and Protection, School of Radiation Medicine and Protection, Collaborative Innovation Center of Radiological Medicine of Jiangsu Higher Education Institutions, Soochow University, Suzhou 215123, China 
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Abstract::
      Given the pervasive utilization of radiotherapy in the management of thoracic neoplasms, there has been a concomitant rise in the prevalence of radiation-induced lunginjury(RILI)Clinically, RILI is classified into early-stage radiation pneumonitis(RP)and middle-to-late-stage radiation-induced pulmonary fibrosis(RIPF). Among these, RIPF is irreversible and can lead to respiratory dysfunction and even death. Currently, the clinical prevention and treatment drugs in use have limited efficacy, thereby necessitating in-depth exploration of its pathogenesis is urgently needed. Recent studies have indicated thationizing radiation can induce alterations in the pulmonary immune microenvironment, thereby prompting the development of complex interactive regulatory networks among diverse immune cells, including macrophages, T cells, neutrophils, dendritic cells, NK cells, and B cells. These networks are thought to be mediated by cytokines, chemokines, and reactive oxygen species. The onset and progression of RILI is facilitated by this phenomenon. In addition, this network has been shown to drive the progression of pulmonary inflammation and fibrosis by regulating the functions of alveolar epithelial cells, pulmonary vascular endothelial cells, and pulmonary fibroblasts. This article reviews the current understanding of how immune cell interaction networks and the interactions between immune cells and lung parenchymal cells modulate RILI, with the aim of providing essential theoretical foundations for expanding molecular mechanism research on RILI and developing precise intervention strategies.
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