Tumor Cell Death and ATP Release Prime Dendritic Cells and Efficient Anticancer Immunity
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- Laetitia Aymeric
- Authors' Affiliations: 1INSERM, U805; 2Institut Gustave Roussy; 3Université Paris-Sud, Villejuif, France; 4AVENIR team INSERM CRI-866; 5Centre Georges Francois Leclerc, Dijon, France; 6INSERM, U848, Villejuif, France; and 7Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
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- Lionel Apetoh
- Authors' Affiliations: 1INSERM, U805; 2Institut Gustave Roussy; 3Université Paris-Sud, Villejuif, France; 4AVENIR team INSERM CRI-866; 5Centre Georges Francois Leclerc, Dijon, France; 6INSERM, U848, Villejuif, France; and 7Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
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- François Ghiringhelli
- Authors' Affiliations: 1INSERM, U805; 2Institut Gustave Roussy; 3Université Paris-Sud, Villejuif, France; 4AVENIR team INSERM CRI-866; 5Centre Georges Francois Leclerc, Dijon, France; 6INSERM, U848, Villejuif, France; and 7Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
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- Antoine Tesniere
- Authors' Affiliations: 1INSERM, U805; 2Institut Gustave Roussy; 3Université Paris-Sud, Villejuif, France; 4AVENIR team INSERM CRI-866; 5Centre Georges Francois Leclerc, Dijon, France; 6INSERM, U848, Villejuif, France; and 7Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
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- Isabelle Martins
- Authors' Affiliations: 1INSERM, U805; 2Institut Gustave Roussy; 3Université Paris-Sud, Villejuif, France; 4AVENIR team INSERM CRI-866; 5Centre Georges Francois Leclerc, Dijon, France; 6INSERM, U848, Villejuif, France; and 7Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
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- Guido Kroemer
- Authors' Affiliations: 1INSERM, U805; 2Institut Gustave Roussy; 3Université Paris-Sud, Villejuif, France; 4AVENIR team INSERM CRI-866; 5Centre Georges Francois Leclerc, Dijon, France; 6INSERM, U848, Villejuif, France; and 7Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
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- Mark J. Smyth
- Authors' Affiliations: 1INSERM, U805; 2Institut Gustave Roussy; 3Université Paris-Sud, Villejuif, France; 4AVENIR team INSERM CRI-866; 5Centre Georges Francois Leclerc, Dijon, France; 6INSERM, U848, Villejuif, France; and 7Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
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- Laurence Zitvogel
- Authors' Affiliations: 1INSERM, U805; 2Institut Gustave Roussy; 3Université Paris-Sud, Villejuif, France; 4AVENIR team INSERM CRI-866; 5Centre Georges Francois Leclerc, Dijon, France; 6INSERM, U848, Villejuif, France; and 7Cancer Immunology Program, Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
説明
<jats:title>Abstract</jats:title> <jats:p>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 γ (IFNγ) and the IFNγ 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-1β (IL-1β). IL-1β then is required for the adequate polarization of IFNγ-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</jats:p>
収録刊行物
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- Cancer Research
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Cancer Research 70 (3), 855-858, 2010-01-31
American Association for Cancer Research (AACR)
