Cell Death and Aging Team, Gystave Roussy Cancer Campus, Villejuif, France; Laboratory of Molecular Radiotherapy, INSERM U1030, Gystave Roussy Cancer Campus, Villejuif, France; Gystave Roussy Cancer Campus, Villejuif, France; Université Paris Sud - Paris Saclay, Villejuif, France; Department of Radiation and Medical Oncology, Zhongnan Hospital, Wuhan University, Hubei, China; Hubei Key Laboratory of Tumor Biological Behaviors, Zhongnan Hospital, Wuhan University, Hubei, China.
Cell Death and Aging Team, Gystave Roussy Cancer Campus, Villejuif, France; Laboratory of Molecular Radiotherapy, INSERM U1030, Gystave Roussy Cancer Campus, Villejuif, France; Gystave Roussy Cancer Campus, Villejuif, France; Université Paris Sud - Paris Saclay, Villejuif, France.
Biomed J. 2017 Aug;40(4):200-211. doi: 10.1016/j.bj.2017.06.003. Epub 2017 Jul 29.
Radiation therapy is one of the major therapeutic modalities for most solid tumors. The anti-tumor effect of radiation therapy consists of the direct tumor cell killing, as well as the modulation of tumor microenvironment and the activation of immune response against tumors. Radiation therapy has been shown to promote immunogenic cells death, activate dendritic cells and enhance tumor antigen presentation and anti-tumor T cell activation. Radiation therapy also programs innate immune cells such as macrophages that leads to either radiosensitization or radioresistance, according to different tumors and different radiation regimen studied. The mechanisms underlying radiation-induced macrophage activation remain largely elusive. Various molecular players such as NF-κB, MAPKs, p53, reactive oxygen species, inflammasomes have been involved in these processes. The skewing to a pro-inflammatory phenotype thus results in the activation of anti-tumor immune response and enhanced radiotherapy effect. Therefore, a comprehensive understanding of the mechanism of radiation-induced macrophage activation and its role in tumor response to radiation therapy is crucial for the development of new therapeutic strategies to enhance radiation therapy efficacy.
放射治疗是大多数实体瘤的主要治疗方法之一。放射治疗的抗肿瘤作用包括直接杀伤肿瘤细胞，以及调节肿瘤微环境和激活针对肿瘤的免疫反应。放射治疗已被证明可促进免疫原性细胞死亡，激活树突状细胞，并增强肿瘤抗原呈递和抗肿瘤 T 细胞激活。根据不同的肿瘤和不同的放射治疗方案，放射治疗还可对巨噬细胞等固有免疫细胞进行编程，从而导致放射增敏或放射抵抗。放射诱导的巨噬细胞激活的机制在很大程度上仍不清楚。各种分子参与者，如 NF-κB、MAPKs、p53、活性氧、炎性小体，都参与了这些过程。向促炎表型的倾斜导致抗肿瘤免疫反应的激活和放射治疗效果的增强。因此，全面了解放射诱导的巨噬细胞激活的机制及其在肿瘤对放射治疗反应中的作用，对于开发增强放射治疗效果的新治疗策略至关重要。
