辐射是地球环境的普遍组成部分，分为非电离形式和电离形式。虽然非电离辐射相对无害，但电离辐射拥有足够的能量来电离原子并破坏 DNA，从而导致细胞损伤、突变、癌症和细胞死亡。放射性核素和电离辐射在核技术和医疗应用中的广泛使用引起了全球对其引起急性和慢性疾病的能力的关注。电离辐射直接通过链断裂和碱基变化诱导 DNA 损伤，或通过水的辐射分解产生活性氧 (ROS) 和活性氮 (RNS) 间接诱导 DNA 损伤。这种损伤会引发复杂的细胞反应，包括识别 DNA 损伤、细胞周期停滞、DNA 修复机制、促炎细胞因子的释放和细胞死亡。本综述重点关注辐射引起的细胞损伤的机制、DNA 损伤的识别和随后的修复过程激活，以及先天免疫反应在损伤修复中的关键作用。重点放在模式识别受体（PRR）和检测损伤相关分子模式（DAMP）并启动下游信号通路的相关受体上。详细讨论了辐射诱导的细胞死亡途径。了解这些过程对于制定减轻辐射有害影响和改善治疗结果的策略至关重要。© 2024 作者。约翰·威利出版的免疫学评论

Radiation, a universal component of Earth's environment, is categorized into non-ionizing and ionizing forms. While non-ionizing radiation is relatively harmless, ionizing radiation possesses sufficient energy to ionize atoms and disrupt DNA, leading to cell damage, mutation, cancer, and cell death. The extensive use of radionuclides and ionizing radiation in nuclear technology and medical applications has sparked global concern for their capacity to cause acute and chronic illnesses. Ionizing radiation induces DNA damage either directly through strand breaks and base change or indirectly by generating reactive oxygen species (ROS) and reactive nitrogen species (RNS) via radiolysis of water. This damage triggers a complex cellular response involving recognition of DNA damage, cell cycle arrest, DNA repair mechanisms, release of pro-inflammatory cytokines, and cell death. This review focuses on the mechanisms of radiation-induced cellular damage, recognition of DNA damage and subsequent activation of repair processes, and the critical role of the innate immune response in resolution of the injury. Emphasis is placed on pattern recognition receptors (PRRs) and related receptors that detect damage-associated molecular patterns (DAMPs) and initiate downstream signaling pathways. Radiation-induced cell death pathways are discussed in detail. Understanding these processes is crucial for developing strategies to mitigate the harmful effects of radiation and improve therapeutic outcomes.© 2024 The Author(s). Immunological Reviews published by John Wiley & Sons Ltd.