1. Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1.
- Author
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Vacchelli, Erika, Yuting Ma, Baracco, Elisa E., Sistigu, Antonella, Enot, David P., Pietrocola, Federico, Heng Yang, Adjemian, Sandy, Chaba, Kariman, Semeraro, Michaela, Signore, Michele, dele De Ninno, A., Lucarini, Valeria, Peschiaroli, Francesca, Businaro, Luca, Gerardino, Annamaria, Manic, Gwenola, Ulas, Thomas, Günther, Patrick, and Schultze, Joachim L.
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DENDRITIC cells , *ANTINEOPLASTIC agents , *CANCER chemotherapy , *CANCER treatment , *IMMUNE response , *T cells , *BREAST cancer patients , *COLON cancer patients - 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. [ABSTRACT FROM AUTHOR]
- Published
- 2015
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