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Tumor stress, cell death and the ensuing immune response.

机译:肿瘤应激,细胞死亡和随之而来的免疫反应。

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摘要

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.Cell Death and Differentiation (2008) 15, 21-28; doi:10.1038/sj.cdd.4402266; published online 9 November 2007.
机译:包括抗癌化学疗法和放射疗法在内的生理和病理情况的聚宝盆可以诱导细胞死亡。然而,肿瘤细胞死亡的免疫学后果仍然很大。关于其各自的免疫原性,反对“凋亡与坏死”的范例目前尚不能预测长期免疫。此外,值得强调的是,肿瘤细胞可能在死亡前被“压迫”,以被免疫细胞识别。受应激的肿瘤在细胞毒性化合物的压力下释放的“吃我”,“危险”和“杀死”信号可能是化疗引起的肿瘤细胞反应与后续免疫反应之间的联系。这篇综述将概述癌症免疫的最新技术,并描述肿瘤细胞死亡如何决定先天免疫与获得性免疫之间的联系。《细胞死亡与分化》(2008)15,21-28; doi:10.1038 / sj.cdd.4402266;在线发布于2007年11月9日。

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