| First Author | Vacchelli E | Year | 2015 |
| Journal | Science | Volume | 350 |
| Issue | 6263 | Pages | 972-8 |
| PubMed ID | 26516201 | Mgi Jnum | J:227052 |
| Mgi Id | MGI:5699620 | Doi | 10.1126/science.aad0779 |
| Citation | Vacchelli E, et al. (2015) Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1. Science 350(6263):972-8 |
| abstractText | 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. |
