Campbell Allison M, Decker Roy H
Oncology (Williston Park). 2018 Jul 15;32(7):370-4, CV3.
In this article, we discuss the immunogenicity of radiation-induced cell death and describe the innate immune signaling pathways that precede adaptive antitumoral immunity. The innate and adaptive immune systems work in concert to generate systemic immune responses. In the setting of cancer, DNA damage caused by radiotherapy activates the innate immune system while tumor cell death liberates antigen that serves as a target for adaptive immunity. The immunomodulatory effects of radiation have been investigated in preclinical models; here we summarize the available data, with particular attention to the effects of radiotherapy timing, location, dose, and fractionation strategy on the antitumoral immune response. We synthesize preclinical and clinical information regarding the potential superiority of hypofractionated radiation for induction of proinflammatory responses. Although many questions remain, early successes with combining immunotherapy and radiotherapy merit further inquiry into the dose and fractionation strategies best able to activate and sustain an antitumoral response.
在本文中，我们讨论了辐射诱导的细胞死亡的免疫原性，并描述了在适应性抗肿瘤免疫之前的固有免疫信号通路。固有免疫系统和适应性免疫系统协同工作以产生全身性免疫反应。在癌症背景下，放疗引起的DNA损伤激活固有免疫系统，而肿瘤细胞死亡释放出作为适应性免疫靶点的抗原。辐射的免疫调节作用已在临床前模型中进行了研究；在此我们总结现有数据，特别关注放疗时间、部位、剂量和分割策略对抗肿瘤免疫反应的影响。我们综合了关于大分割放疗在诱导促炎反应方面潜在优势的临床前和临床信息。尽管仍有许多问题，但免疫疗法与放疗联合的早期成功值得进一步探究最能激活和维持抗肿瘤反应的剂量和分割策略。
