| Literature DB >> 32361713 |
Michael Klichinsky1,2,3, Marco Ruella1,4, Olga Shestova1, Xueqing Maggie Lu1,5, Andrew Best1,3, Martha Zeeman3, Maggie Schmierer3, Konrad Gabrusiewicz3, Nicholas R Anderson3, Nicholas E Petty1, Katherine D Cummins1, Feng Shen1, Xinhe Shan1, Kimberly Veliz1, Kristin Blouch1, Yumi Yashiro-Ohtani3, Saad S Kenderian1,6, Miriam Y Kim1,7, Roddy S O'Connor1, Stephen R Wallace1, Miroslaw S Kozlowski1, Dylan M Marchione2,8, Maksim Shestov1, Benjamin A Garcia8, Carl H June1,2,9, Saar Gill10,11,12.
Abstract
Chimeric antigen receptor (CAR) T cell therapy has shown promise in hematologic malignancies, but its application to solid tumors has been challenging1-4. Given the unique effector functions of macrophages and their capacity to penetrate tumors5, we genetically engineered human macrophages with CARs to direct their phagocytic activity against tumors. We found that a chimeric adenoviral vector overcame the inherent resistance of primary human macrophages to genetic manipulation and imparted a sustained pro-inflammatory (M1) phenotype. CAR macrophages (CAR-Ms) demonstrated antigen-specific phagocytosis and tumor clearance in vitro. In two solid tumor xenograft mouse models, a single infusion of human CAR-Ms decreased tumor burden and prolonged overall survival. Characterization of CAR-M activity showed that CAR-Ms expressed pro-inflammatory cytokines and chemokines, converted bystander M2 macrophages to M1, upregulated antigen presentation machinery, recruited and presented antigen to T cells and resisted the effects of immunosuppressive cytokines. In humanized mouse models, CAR-Ms were further shown to induce a pro-inflammatory tumor microenvironment and boost anti-tumor T cell activity.Entities:
Mesh:
Year: 2020 PMID: 32361713 PMCID: PMC7883632 DOI: 10.1038/s41587-020-0462-y
Source DB: PubMed Journal: Nat Biotechnol ISSN: 1087-0156 Impact factor: 54.908