Cancer cell-autonomous contribution of type I interferon signaling to the efficacy of chemotherapy View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2014-11

AUTHORS

Antonella Sistigu, Takahiro Yamazaki, Erika Vacchelli, Kariman Chaba, David P Enot, Julien Adam, Ilio Vitale, Aicha Goubar, Elisa E Baracco, Catarina Remédios, Laetitia Fend, Dalil Hannani, Laetitia Aymeric, Yuting Ma, Mireia Niso-Santano, Oliver Kepp, Joachim L Schultze, Thomas Tüting, Filippo Belardelli, Laura Bracci, Valentina La Sorsa, Giovanna Ziccheddu, Paola Sestili, Francesca Urbani, Mauro Delorenzi, Magali Lacroix-Triki, Virginie Quidville, Rosa Conforti, Jean-Philippe Spano, Lajos Pusztai, Vichnou Poirier-Colame, Suzette Delaloge, Frederique Penault-Llorca, Sylvain Ladoire, Laurent Arnould, Joanna Cyrta, Marie-Charlotte Dessoliers, Alexander Eggermont, Marco E Bianchi, Mikael Pittet, Camilla Engblom, Christina Pfirschke, Xavier Préville, Gilles Uzè, Robert D Schreiber, Melvyn T Chow, Mark J Smyth, Enrico Proietti, Fabrice André, Guido Kroemer, Laurence Zitvogel

ABSTRACT

Some of the anti-neoplastic effects of anthracyclines in mice originate from the induction of innate and T cell-mediated anticancer immune responses. Here we demonstrate that anthracyclines stimulate the rapid production of type I interferons (IFNs) by malignant cells after activation of the endosomal pattern recognition receptor Toll-like receptor 3 (TLR3). By binding to IFN-α and IFN-β receptors (IFNARs) on neoplastic cells, type I IFNs trigger autocrine and paracrine circuitries that result in the release of chemokine (C-X-C motif) ligand 10 (CXCL10). Tumors lacking Tlr3 or Ifnar failed to respond to chemotherapy unless type I IFN or Cxcl10, respectively, was artificially supplied. Moreover, a type I IFN-related signature predicted clinical responses to anthracycline-based chemotherapy in several independent cohorts of patients with breast carcinoma characterized by poor prognosis. Our data suggest that anthracycline-mediated immune responses mimic those induced by viral pathogens. We surmise that such 'viral mimicry' constitutes a hallmark of successful chemotherapy. More... »

PAGES

1301-1309

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/nm.3708

    DOI

    http://dx.doi.org/10.1038/nm.3708

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1034226043

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/25344738


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