Desirable cell death during anticancer chemotherapy
Desirable cell death during anticancer chemotherapy
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DOI：
10.1111/j.1749-6632.2010.05763.x
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发表时间：
2010-01-01
期刊：
影响因子：
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通讯作者：
Zitvogel, Laurence
中科院分区：
文献类型：
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作者：
Locher, Clara;Conforti, Rosa;Zitvogel, Laurence
最近出现的免疫原性化疗的概念依赖于一种细胞毒性化合物触发细胞死亡模式的能力。这种方式引起树突状细胞对肿瘤抗原特异性T细胞的交叉激发，这将有助于该化合物的杀瘤活性，并保护宿主防止复发。相比之下，大多数抗癌药物诱导的非免疫原性细胞凋亡并不伴随免疫特性。本综述将讨论肿瘤水平所需的一些分子和代谢变化，这些变化必须在宿主水平上参与关键通路，以在化疗期间诱导Tc1极化保护性T细胞反应。我们将综述能增强细胞死亡免疫原性的免疫佐剂，以增强化疗的疗效。
The concept of immunogenic chemotherapy that has recently emerged relies upon the capacity of a cytotoxic compound to trigger a cell-death modality. This modality elicits cross-priming by dendritic cells of tumor antigen-specific T cells that will contribute to the tumoricidal activity of the compound and protect the host against relapse. In contrast, most anticancer drugs elicit nonimmunogenic apoptosis that is not accompanied with an immunizing property. This review will discuss some molecular and metabolic changes required at the level of the tumor that must engage key pathways at the level of the host for the induction of Tc1 polarized protective T cell responses during chemotherapy. We will summarize the immune adjuvants that can boost the immunogenicity of cell death to augment the efficacy of chemotherapy.