Ullrich E, Bonmort M, Mignot G, Kroemer G, Zitvogel L
INSERM U805, Institut Gustave Roussy, Pavillon de Recherche 1, 39 rue Camille Desmoulins, Villejuif, France.
Cell Death Differ. 2008 Jan;15(1):21-8. doi: 10.1038/sj.cdd.4402266. Epub 2007 Nov 9.
A cornucopia of physiological and pathological circumstances including anticancer chemotherapy and radiotherapy can induce cell death. However, the immunological consequences of tumor cell demise have remained largely elusive. The paradigm opposing 'apoptosis versus necrosis' as to their respective immunogenicity does not currently hold to predict long-term immunity. Moreover, the notion that tumor cells may be 'stressed' before death to be recognized by immune cells deserves to be underlined. 'Eat-me', 'danger' and 'killing' signals released by stressed tumor under the pressure of cytotoxic compounds may serve as links between the chemotherapy-elicited response of tumor cells and subsequent immune responses. This review will summarize the state-of-the-art of cancer immunity and describe how tumor cell death dictates the links between innate and acquired immunity.
包括抗癌化疗和放疗在内的大量生理和病理情况均可诱导细胞死亡。然而,肿瘤细胞死亡的免疫后果在很大程度上仍不明确。关于“凋亡与坏死”各自免疫原性的对立范式目前并不适用于预测长期免疫。此外,肿瘤细胞在死亡前可能处于“应激”状态从而被免疫细胞识别这一观点值得强调。在细胞毒性化合物的压力下,应激肿瘤释放的“吃我”“危险”和“杀伤”信号可能是肿瘤细胞化疗引发的反应与后续免疫反应之间的联系。本综述将总结癌症免疫的最新进展,并描述肿瘤细胞死亡如何决定先天免疫和获得性免疫之间的联系。