{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,20]],"date-time":"2026-09-20T13:14:08Z","timestamp":1789910048102,"version":"4.0.1"},"reference-count":80,"publisher":"Oxford University Press (OUP)","issue":"10","license":[{"start":{"date-parts":[[2018,5,1]],"date-time":"2018-05-01T00:00:00Z","timestamp":1525132800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,5,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The transferrin receptor 1 (TfR1) is an attractive target for Ab-mediated cancer therapy. We previously developed a mouse\/human chimeric IgG3 Ab (ch128.1) targeting human TfR1, which exhibits direct in vitro cytotoxicity against certain human malignant B cells through TfR1 degradation and iron deprivation. ch128.1 also demonstrates exceptional antitumor activity against the B cell malignancy multiple myeloma (MM) in xenograft models of SCID-Beige mice bearing either disseminated ARH-77 or KMS-11 cells in an early disease setting. Interestingly, this activity is observed even against KMS-11 cells, which show no sensitivity to the direct cytotoxic activity of ch128.1 in vitro. To understand the contributions of the Fc fragment, we generated a ch128.1 mutant with impaired binding to Fc\u03b3Rs and to the complement component C1q, which retains binding to the neonatal Fc receptor. We now report that this mutant Ab does not show antitumor activity in these two MM models, indicating a crucial role of the Fc fragment in the antitumor activity of ch128.1, which can be attributed to effector functions (Ab-dependent cell-mediated cytotoxicity, Ab-dependent cell-mediated phagocytosis, and\/or complement-dependent cytotoxicity). Interestingly, in the KMS-11 model, complement depletion does not affect protection, whereas macrophage depletion does. Consistent with this observation, we found that ch128.1 induces Ab-dependent cell-mediated cytotoxicity and Ab-dependent cell-mediated phagocytosis against KMS-11 cells in the presence of murine bone marrow\u2013derived macrophages. Finally, we found that ch128.1 therapy effectively increases survival in a late MM disease setting. Our results suggest that macrophages play a major role in ch128.1-mediated antitumor protection in our models and that ch128.1 can be effective against human B cell malignancies such as MM.<\/jats:p>","DOI":"10.4049\/jimmunol.1700787","type":"journal-article","created":{"date-parts":[[2018,4,13]],"date-time":"2018-04-13T18:36:20Z","timestamp":1523644580000},"page":"3485-3494","source":"Crossref","is-referenced-by-count":27,"title":["Efficacy and Mechanism of Antitumor Activity of an Antibody Targeting Transferrin Receptor 1 in Mouse Models of Human Multiple Myeloma"],"prefix":"10.1093","volume":"200","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-0932-4872","authenticated-orcid":false,"given":"Lai Sum","family":"Leoh","sequence":"first","affiliation":[{"name":"Division of Surgical Oncology, Department of Surgery, David Geffen School of Medicine at UCLA , Los Angeles, CA 90095"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yoon Kyung","family":"Kim","sequence":"additional","affiliation":[{"name":"Division of Surgical Oncology, Department of Surgery, David Geffen School of Medicine at UCLA , Los Angeles, CA 90095"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pierre V","family":"Candelaria","sequence":"additional","affiliation":[{"name":"Division of Surgical Oncology, Department of Surgery, David Geffen School of Medicine at UCLA , Los Angeles, CA 90095"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1364-0675","authenticated-orcid":false,"given":"Otoniel","family":"Mart\u00ednez-Maza","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine at UCLA , Los Angeles, CA 90095"},{"name":"Jonsson Comprehensive Cancer Center, University of California, Los Angeles , Los Angeles, CA 90095"},{"name":"Department of Obstetrics and Gynecology, David Geffen School of Medicine at UCLA , Los Angeles, CA 90095"},{"name":"Department of Epidemiology, Jonathan and Karin Fielding School of Public Health, University of California, Los Angeles , Los Angeles, CA 90095"},{"name":"UCLA AIDS Institute , Los Angeles, CA 90024"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8277-9702","authenticated-orcid":false,"given":"Tracy R","family":"Daniels-Wells","sequence":"additional","affiliation":[{"name":"Division of Surgical Oncology, Department of Surgery, David Geffen School of Medicine at UCLA , Los Angeles, CA 90095"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Manuel L","family":"Penichet","sequence":"additional","affiliation":[{"name":"Division of Surgical Oncology, Department of Surgery, David Geffen School of Medicine at UCLA , Los Angeles, CA 90095"},{"name":"Department of Microbiology, Immunology, and Molecular Genetics, David Geffen School of Medicine at UCLA , Los Angeles, CA 90095"},{"name":"Jonsson Comprehensive Cancer Center, University of California, Los Angeles , Los Angeles, CA 90095"},{"name":"UCLA AIDS Institute , Los Angeles, CA 90024"},{"name":"The Molecular Biology Institute, University of California, Los Angeles , Los Angeles, CA 90095"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2018,5,15]]},"reference":[{"key":"2025030610150111600_r1","doi-asserted-by":"crossref","first-page":"7","DOI":"10.3322\/caac.21387","article-title":"Cancer statistics, 2017","volume":"67","author":"Siegel","year":"2017","journal-title":"CA Cancer J. 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