| First Author | Albanesi M | Year | 2013 |
| Journal | Blood | Volume | 122 |
| Issue | 18 | Pages | 3160-4 |
| PubMed ID | 23980063 | Mgi Jnum | J:203437 |
| Mgi Id | MGI:5527026 | Doi | 10.1182/blood-2013-04-497446 |
| Citation | Albanesi M, et al. (2013) Neutrophils mediate antibody-induced antitumor effects in mice. Blood 122(18):3160-4 |
| abstractText | Tumor engraftment followed by monoclonal antibody (mAb) therapy targeting tumor antigens represents a gold standard for assessing the efficiency of mAbs to eliminate tumor cells. Mouse models have demonstrated that receptors for the Fc portion of immunoglobulin G (FcgammaRs) are critical determinants of mAb therapeutic efficacy, but the FcgammaR-expressing cell populations responsible remain elusive. We show that neutrophils are responsible for mAb-induced therapy of both subcutaneous syngeneic melanoma and human breast cancer xenografts. mAb-induced tumor reduction, abolished in neutropenic mice, could be restored in FcgammaR-deficient hosts upon transfer of FcgammaR+ neutrophils or upon human FcgammaRIIA/CD32A transgenic expression. Finally, conditional knockout mice unable to perform FcgammaR-mediated activation and phagocytosis specifically in neutrophils were resistant to mAb-induced therapy. Our work suggests that neutrophils are necessary and sufficient for mAb-induced therapy of subcutaneous tumors, and represent a new and critical focal point for optimizing mAb-induced immunotherapies that will impact on human cancer treatment. |
