期刊
SCIENCE
卷 350, 期 6263, 页码 972-978出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aad0779
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资金
- Ligue Nationale Contre le Cancer (Equipes Labellisees)
- Sites de Recherche Integrees sur le Cancer (SIRIC) Socrates and Carpem
- Swiss Institute for Experimental Cancer Research (ISREC) Foundation
- Agence Nationale pour la Recherche (AUTOPH, Emergence)
- Canceropole Ile-de-France
- European Commission (ArtForce)
- European Research Council
- Fondation pour la Recherche Medicale
- Fondation de France
- LabEx Immuno-Oncology
- Institut National du Cancer (INCa)
- Paris Alliance of Cancer Research Institutes
- LabEx Immuno-Oncologie
- Chinese National Thousand Talents Program
- Deutsche Forschungsgemeinschaft [SFB704, SFB645]
- Excellence Cluster ImmunoSensation
- Italian Ministry of Health [RF-2011-02347120]
- Associazione Italiana per la Ricerca sul Cancro (AIRC) [IG 14297]
- AIRC [MFAG 14641]
- Italian Ministry of Health
- Programma per i Giovani Ricercatori Rita Levi Montalcini
- AIRC
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.
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