| Literature DB >> 26516201 |
Erika Vacchelli1, Yuting Ma2, Elisa E Baracco3, Antonella Sistigu4, David P Enot5, Federico Pietrocola3, Heng Yang2, Sandy Adjemian6, Kariman Chaba7, Michaela Semeraro8, Michele Signore9, Adele De Ninno10, Valeria Lucarini9, Francesca Peschiaroli9, Luca Businaro10, Annamaria Gerardino10, Gwenola Manic4, Thomas Ulas11, Patrick Günther11, Joachim L Schultze11, Oliver Kepp1, Gautier Stoll1, Céline Lefebvre12, Claire Mulot13, Francesca Castoldi14, Sylvie Rusakiewicz8, Sylvain Ladoire15, Lionel Apetoh15, José Manuel Bravo-San Pedro1, Monica Lucattelli16, Cécile Delarasse17, Valérie Boige18, Michel Ducreux19, Suzette Delaloge20, Christophe Borg21, Fabrice André22, Giovanna Schiavoni9, Ilio Vitale23, Pierre Laurent-Puig24, Fabrizio Mattei9, Laurence Zitvogel25, Guido Kroemer26.
Abstract
Antitumor immunity driven by intratumoral dendritic cells contributes to the efficacy of anthracycline-based chemotherapy in cancer. We identified a loss-of-function allele of the gene coding for formyl peptide receptor 1 (FPR1) that was associated with poor metastasis-free and overall survival in breast and colorectal cancer patients receiving adjuvant chemotherapy. The therapeutic effects of anthracyclines were abrogated in tumor-bearing Fpr1(-/-) mice due to impaired antitumor immunity. Fpr1-deficient dendritic cells failed to approach dying cancer cells and, as a result, could not elicit antitumor T cell immunity. Experiments performed in a microfluidic device confirmed that FPR1 and its ligand, annexin-1, promoted stable interactions between dying cancer cells and human or murine leukocytes. Altogether, these results highlight the importance of FPR1 in chemotherapy-induced anticancer immune responses.Entities:
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Year: 2015 PMID： 26516201 DOI： 10.1126/science.aad0779
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728