期刊
CANCER RESEARCH
卷 70, 期 3, 页码 855-858出版社
AMER ASSOC CANCER RESEARCH
DOI: 10.1158/0008-5472.CAN-09-3566
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资金
- Ligue Nationale contre le Cancer
- European Union
- Fondation pour la Recherche Medicale
- Canceropole Ile-de-France
- Institut National du Cancer
- Association for International Cancer Research
- Agence Nationale pour la Recherche
- National Health and Medical Research Council of Australia
- Victorian Cancer Agency
- INSERM
By destroying tumor cells, conventional anticancer therapies may stimulate the host immune system to eliminate residual disease. Anthracyclines, oxaliplatin, and ionizing irradiation activate a type of tumor cell death that elicits efficient anticancer immune responses depending on interferon gamma(IFN gamma) and the IFN gamma receptor. Thus, dying tumor cells emit danger signals that are perceived by dendritic cells (DC), which link innate and cognate immune responses. Recently, we observed that ATP was released by tumor cells succumbing to chemotherapy. ATP activates purinergic P2RX7 receptors on DC, thus activating the NLRP3/ASC/caspase-1 inflammasome and driving the secretion of interleukin-1 beta (IL-1 beta). IL-1 beta then is required for the adequate polarization of IFN gamma-producing CD8(+) T cells. These results imply a novel danger signal, ATP, and a novel receptor, P2RX7, in the chemotherapy-elicited anticancer immune response. Cancer Res; 70(3); 855-8. (C)2010 AACR.
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