{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,8]],"date-time":"2026-09-08T12:46:14Z","timestamp":1788871574977,"version":"build-2803163510"},"reference-count":22,"publisher":"Oxford University Press (OUP)","issue":"5","license":[{"start":{"date-parts":[[2010,7,27]],"date-time":"2010-07-27T00:00:00Z","timestamp":1280188800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"funder":[{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"publisher","award":["MOP 37490"],"award-info":[{"award-number":["MOP 37490"]}],"id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100000038","name":"Natural Sciences Engineering Research council","doi-asserted-by":"crossref","id":[{"id":"10.13039\/501100000038","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2010,7,27]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Antibody-dependent cellular cytotoxicity levels reflect a formative interaction between killer cell immunoglobulin-like receptor 3DL1 and the class I human leukocyte antigen Bw4 epitope.<\/jats:p>\n                  <jats:p>Activating receptor-mediated recognition of stress-induced ligands or IgG antibody bridging of tumor or pathogen-associated antigens to the Fc\u03b3RIII CD16 triggers NK cells to kill transformed and infected cells with reduced HLA-I expression. According to the licensing hypothesis, NK cells become competent for activating receptor-mediated triggering after a formative encounter between a NK inhibitory receptor and its ligand. This general hypothesis is supported by murine and human studies, but to date, evidence of a role for such licensing in human ADCC is ambiguous. Inhibitory receptor interactions with HLA-C promote NK cell ADCC licensing, but interactions between KIR3DL1 and its HLA-Bw4 ligand may be insufficient. We investigated the impact of KIR3DL1 and HLA-Bw4 coexpression on NK cell ADCC using a robust, genuine target system of antibody-bearing EBV-transformed B lymphocytes. Although numbers of KIR3DL1+ NK cells were similar in HLA-Bw4+ and HLA-Bw4\u2013 individuals, general levels of ADCC mediated against target cells were significantly higher in a group of HLA-Bw4+KIR3DL1+ individuals than in a comparable HLA-Bw4\u2013 group. Flow cytometry demonstrated directly that a significantly higher fraction of KIR3DL1+ NK cells derived from HLA-Bw4+ compared with HLA-Bw4\u2013 individuals produced IFN-\u03b3 following stimulation with ADCC targets. Murine FcR-bearing P815 target cells also triggered higher levels of CD16-mediated cytotoxicity by NK cells from HLA-Bw4+KIR3DL1+ individuals. These results indicate a prominent role for KIR3DL1\/HLA-Bw4 interactions in licensing NK cells for CD16-mediated effector function.<\/jats:p>","DOI":"10.1189\/jlb.1009687","type":"journal-article","created":{"date-parts":[[2010,7,27]],"date-time":"2010-07-27T22:30:22Z","timestamp":1280269822000},"page":"905-912","source":"Crossref","is-referenced-by-count":43,"title":["Killer cell immunoglobulin-like receptor 3DL1 licenses CD16-mediated effector functions of natural killer cells"],"prefix":"10.1093","volume":"88","author":[{"given":"Matthew S","family":"Parsons","sequence":"first","affiliation":[{"name":"Immunology and Infectious Disease Program, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland , St. John\u02c8s, Newfoundland & Labrador, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Katrin","family":"Zipperlen","sequence":"additional","affiliation":[{"name":"Immunology and Infectious Disease Program, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland , St. John\u02c8s, Newfoundland & Labrador, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maureen","family":"Gallant","sequence":"additional","affiliation":[{"name":"Immunology and Infectious Disease Program, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland , St. John\u02c8s, Newfoundland & Labrador, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael","family":"Grant","sequence":"additional","affiliation":[{"name":"Immunology and Infectious Disease Program, Division of BioMedical Sciences, Faculty of Medicine, Memorial University of Newfoundland , St. John\u02c8s, Newfoundland & Labrador, Canada"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2010,7,27]]},"reference":[{"key":"2023032712205273000_jlb0905-cit-b1","doi-asserted-by":"crossref","first-page":"2711","DOI":"10.1002\/1521-4141(2002010)32:10<2711::AID-IMMU2711>3.0.CO;2-3","article-title":"NK cell activity controls human herpesvirus 8 latent infection and is restored upon highly active antiretroviral therapy in AIDS patents with regressing Kaposi's sarcoma","volume":"32","author":"Sirianni","year":"2002","journal-title":"Eur. 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