| 曹诗雯,焦旸.免疫细胞互作网络调控放射性肺损伤的机制研究进展[J].中华放射医学与防护杂志,2026,46(5):547-554.Cao Shiwen,Jiao Yang.Progress in research on the mechanism of immune cell interaction networks in regulating radiation-induced lung injury[J].Chin J Radiol Med Prot,2026,46(5):547-554 |
| 免疫细胞互作网络调控放射性肺损伤的机制研究进展 |
| Progress in research on the mechanism of immune cell interaction networks in regulating radiation-induced lung injury |
| 投稿时间：2025-07-15 |
| DOI：10.3760/cma.j.cn112271-20250715-00250 |
| 中文关键词: 电离辐射 免疫微环境 细胞间相互作用 放射性肺炎 放射性肺纤维化 |
| 英文关键词:Ionizing radiation Immune microenvironment Intercellular interactions Radiation pneumonitis Radiation-induced lung fibrosis |
| 基金项目: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) |
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| 中文摘要: |
| 随着放射治疗在胸部肿瘤中的广泛应用,放射性肺损伤(RILI)的发生率也呈上升趋势。RILI临床分为早期放射性肺炎与中晚期放射性肺纤维化,其中放射性肺纤维化具有不可逆性,可致呼吸功能障碍甚至死亡,目前临床防治药物效果有限,亟需深入探究其发病机制。近年研究表明,电离辐射可改变肺部免疫微环境,促使巨噬细胞、T细胞、中性粒细胞及树突状细胞、NK细胞、B细胞等多种免疫细胞,通过细胞因子、趋化因子和活性氧等形成复杂的交互调控网络,促进RILI的发生与进展。此外,该网络可通过调控肺泡上皮细胞、肺血管内皮细胞及肺成纤维细胞功能,推动肺组织炎症进展与纤维化进程。本文对免疫细胞间以及免疫细胞与肺实质细胞间互作网络调控RILI的机制研究进展进行了概述,以期为拓展RILI发生分子机制学研究及构建精准干预策略提供必要的理论研究依据。 |
| 英文摘要: |
| 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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