Dissemin is shutting down on January 1st, 2025

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American Association for the Advancement of Science, Science, 6263(350), p. 972-978, 2015

DOI: 10.1126/science.aad0779

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Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1

Journal article published in 2015 by Erika Vacchelli ORCID, Yuting Ma, Yuting, Elisa E. Baracco, Antonella Sistigu ORCID, David P. Enot, Federico Pietrocola, Heng Yang, Sandy Adjemian, Kariman Chaba, Michaela Semeraro, Michele Signore ORCID, Adele De Ninno, Valeria Lucarini, Francesca Peschiaroli and other authors.
This paper is available in a repository.
This paper is available in a repository.

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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.