Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1

• Autores: Erika Vacchelli, Yuting Ma, Antonella Sistigu, Federico Pietrocola
• Localización: Science, ISSN 0036-8075, Vol. 350, Nº 6263, 2015, págs. 973-978
• Idioma: inglés
• Texto completo no disponible (Saber más ...)
• Resumen

  • 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.