{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T15:16:46Z","timestamp":1791299806968,"version":"4.1.0"},"reference-count":29,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2015,7]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>In contrast to other antibodies involved in transfusion-related acute lung injury, anti\u2013HNA-3a antibodies are incapable of inducing direct neutrophil activation and seem to interact with endothelial cells (ECs) primarily. In animal studies, anti\u2013HNA-3a-mediated transfusion-related acute lung injury could be precipitated in the absence of neutrophils, but was stronger when neutrophils were present. In a different context the target protein of these antibodies, choline transporter-like protein-2 (CTL-2), was reported to interact with a protein of the inner ear carrying 2 von Willebrand factor (VWF) A-domains. These observations prompted us to investigate whether VWF might be involved in anti\u2013HNA-3a-mediated neutrophil activation, and whether signaling via CD11b\/CD18 is involved, as in various other experimental settings.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Approach and Results\u2014<\/jats:title>\n            <jats:p>Cell adhesion demonstrated specific binding of CTL-2 to VWF. Immunoprecipitation analysis of CTL-2\/CD11b\/CD18 coexpressing cells indicated that anti\u2013HNA-3a colocalizes CTL-2 and CD11b\/CD18 when VWF is present. Functional studies revealed that anti\u2013HNA-3a-mediated neutrophil agglutination is an active, protein kinase C-dependent and partially Fc-dependent process. Agglutination and the production of reactive oxygen species seem to require the formation of a trimolecular complex between the target antigen (CTL-2), CD11b\/CD18 and VWF. In line with these observations, anti\u2013HNA-3a induced less severe transfusion-related acute lung injury and less neutrophil recruitment to the alveolar space in VWF knockout mice.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusions\u2014<\/jats:title>\n            <jats:p>We introduce CTL-2 as a new binding partner for VWF. Interaction of neutrophils with VWF via CTL-2 allows anti\u2013HNA-3a to induce signal transduction via CD11b\/CD18, which leads to neutrophil activation and agglutination. In transfusion-related acute lung injury, this mechanism may further aggravate endothelial leakage.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.115.305259","type":"journal-article","created":{"date-parts":[[2015,5,1]],"date-time":"2015-05-01T01:42:13Z","timestamp":1430444533000},"page":"1616-1622","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":40,"title":["Choline Transporter-Like Protein-2"],"prefix":"10.1161","volume":"35","author":[{"given":"Behnaz","family":"Bayat","sequence":"first","affiliation":[{"name":"From the Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany (B.B., Y.T., H.B., S.W., U.J.S., S.S.); and Laboratory for Thrombosis Research, KU Leuven Kulak, Kortrijk, Belgium (H.D., S.F.D.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yudy","family":"Tjahjono","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany (B.B., Y.T., H.B., S.W., U.J.S., S.S.); and Laboratory for Thrombosis Research, KU Leuven Kulak, Kortrijk, Belgium (H.D., S.F.D.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heike","family":"Bergh\u00f6fer","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany (B.B., Y.T., H.B., S.W., U.J.S., S.S.); and Laboratory for Thrombosis Research, KU Leuven Kulak, Kortrijk, Belgium (H.D., S.F.D.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silke","family":"Werth","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany (B.B., Y.T., H.B., S.W., U.J.S., S.S.); and Laboratory for Thrombosis Research, KU Leuven Kulak, Kortrijk, Belgium (H.D., S.F.D.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hans","family":"Deckmyn","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany (B.B., Y.T., H.B., S.W., U.J.S., S.S.); and Laboratory for Thrombosis Research, KU Leuven Kulak, Kortrijk, Belgium (H.D., S.F.D.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon F.","family":"De Meyer","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany (B.B., Y.T., H.B., S.W., U.J.S., S.S.); and Laboratory for Thrombosis Research, KU Leuven Kulak, Kortrijk, Belgium (H.D., S.F.D.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ulrich J.","family":"Sachs","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany (B.B., Y.T., H.B., S.W., U.J.S., S.S.); and Laboratory for Thrombosis Research, KU Leuven Kulak, Kortrijk, Belgium (H.D., S.F.D.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sentot","family":"Santoso","sequence":"additional","affiliation":[{"name":"From the Institute for Clinical Immunology and Transfusion Medicine, Justus Liebig University, Giessen, Germany (B.B., Y.T., H.B., S.W., U.J.S., S.S.); 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