免疫原性细胞死亡
自噬
免疫系统
程序性细胞死亡
癌细胞
细胞外
免疫原性
癌症研究
三磷酸腺苷
细胞生物学
细胞凋亡
癌症
生物
免疫学
免疫疗法
生物化学
遗传学
作者
Mickaël Michaud,Isabelle Martins,Abdul Qader Sukkurwala,Sandy Adjemian,Yuting Ma,Patrizia Pellegatti,Shensi Shen,Oliver Kepp,Marie Scoazec,Grégoire Mignot,Santiago Rello‐Varona,Maximilien Tailler,Laurie Menger,Erika Vacchelli,Lorenzo Galluzzi,François Ghiringhelli,Francesco Di Virgilio,Laurence Zitvogel,Guido Kroemer
出处
期刊:Science
[American Association for the Advancement of Science (AAAS)]
日期:2011-12-15
卷期号:334 (6062): 1573-1577
被引量:1222
标识
DOI:10.1126/science.1208347
摘要
Antineoplastic chemotherapies are particularly efficient when they elicit immunogenic cell death, thus provoking an anticancer immune response. Here we demonstrate that autophagy, which is often disabled in cancer, is dispensable for chemotherapy-induced cell death but required for its immunogenicity. In response to chemotherapy, autophagy-competent, but not autophagy-deficient, cancers attracted dendritic cells and T lymphocytes into the tumor bed. Suppression of autophagy inhibited the release of adenosine triphosphate (ATP) from dying tumor cells. Conversely, inhibition of extracellular ATP-degrading enzymes increased pericellular ATP in autophagy-deficient tumors, reestablished the recruitment of immune cells, and restored chemotherapeutic responses but only in immunocompetent hosts. Thus, autophagy is essential for the immunogenic release of ATP from dying cells, and increased extracellular ATP concentrations improve the efficacy of antineoplastic chemotherapies when autophagy is disabled.
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