{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T09:44:16Z","timestamp":1791020656223,"version":"4.1.0"},"reference-count":54,"publisher":"Rockefeller University Press","issue":"6","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[1998,9,21]]},"abstract":"<jats:p>The urokinase receptor (CD87; uPAR) is found in close association with \u03b22 integrins on leukocytes. We studied the functional consequence of this association for leukocyte adhesion and migration. In vivo, the \u03b22 integrin\u2013dependent recruitment of leukocytes to the inflamed peritoneum of uPAR-deficient mice was significantly reduced as compared with wild-type animals. In vitro, \u03b22 integrin\u2013mediated adhesion of leukocytes to endothelium was lost upon removal of uPAR from the leukocyte surface by phosphatidyl-inositol\u2013specific phospholipase C. Leukocyte adhesion was reconstituted when soluble intact uPAR, but not a truncated form lacking the uPA-binding domain, was allowed to reassociate with the cell surface. uPAR ligation with a monoclonal antibody induced adhesion of monocytic cells and neutrophils to vascular endothelium by six- to eightfold, whereas ligation with inactivated uPA significantly reduced cell-to-cell adhesion irrespective of the \u03b22 integrin\u2013stimulating pathway. These data indicate that \u03b22 integrin\u2013mediated leukocyte\u2013endothelial cell interactions and recruitment to inflamed areas require the presence of uPAR and define a new phenotype for uPAR-deficient mice. Moreover, uPAR ligation differentially modulates leukocyte adhesion to endothelium and provides novel targets for therapeutic strategies in inflammation-related vascular pathologies.<\/jats:p>","DOI":"10.1084\/jem.188.6.1029","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T16:48:54Z","timestamp":1027702134000},"page":"1029-1037","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":189,"title":["Urokinase Receptor (CD87) Regulates Leukocyte Recruitment via \u03b22 Integrins In Vivo"],"prefix":"10.1084","volume":"188","author":[{"given":"Andreas E.","family":"May","sequence":"first","affiliation":[{"name":"From the *Haemostasis Research Unit, Max-Planck Institute, Kerckhoff-Klinik, D-61231 Bad Nauheim, Germany; the \u2021Finsen Laboratory, Rigshospitalet, DK-2100 Copenhagen, Denmark; the \u00a7Basel Institute for Immunology, CH-4001 Basel, Switzerland; and the \u2016Department of Pathology, Centre Medical Universitaire, CH-1211 Geneva 4, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandip M.","family":"Kanse","sequence":"additional","affiliation":[{"name":"From the *Haemostasis Research Unit, Max-Planck Institute, Kerckhoff-Klinik, D-61231 Bad Nauheim, Germany; the \u2021Finsen Laboratory, Rigshospitalet, DK-2100 Copenhagen, Denmark; the \u00a7Basel Institute for Immunology, CH-4001 Basel, Switzerland; and the \u2016Department of Pathology, Centre Medical Universitaire, CH-1211 Geneva 4, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leif R.","family":"Lund","sequence":"additional","affiliation":[{"name":"From the *Haemostasis Research Unit, Max-Planck Institute, Kerckhoff-Klinik, D-61231 Bad Nauheim, Germany; the \u2021Finsen Laboratory, Rigshospitalet, DK-2100 Copenhagen, Denmark; the \u00a7Basel Institute for Immunology, CH-4001 Basel, Switzerland; and the \u2016Department of Pathology, Centre Medical Universitaire, CH-1211 Geneva 4, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roland H.","family":"Gisler","sequence":"additional","affiliation":[{"name":"From the *Haemostasis Research Unit, Max-Planck Institute, Kerckhoff-Klinik, D-61231 Bad Nauheim, Germany; the \u2021Finsen Laboratory, Rigshospitalet, DK-2100 Copenhagen, Denmark; the \u00a7Basel Institute for Immunology, CH-4001 Basel, Switzerland; and the \u2016Department of Pathology, Centre Medical Universitaire, CH-1211 Geneva 4, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Beat A.","family":"Imhof","sequence":"additional","affiliation":[{"name":"From the *Haemostasis Research Unit, Max-Planck Institute, Kerckhoff-Klinik, D-61231 Bad Nauheim, Germany; the \u2021Finsen Laboratory, Rigshospitalet, DK-2100 Copenhagen, Denmark; the \u00a7Basel Institute for Immunology, CH-4001 Basel, Switzerland; and the \u2016Department of Pathology, Centre Medical Universitaire, CH-1211 Geneva 4, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Klaus T.","family":"Preissner","sequence":"additional","affiliation":[{"name":"From the *Haemostasis Research Unit, Max-Planck Institute, Kerckhoff-Klinik, D-61231 Bad Nauheim, Germany; the \u2021Finsen Laboratory, Rigshospitalet, DK-2100 Copenhagen, Denmark; the \u00a7Basel Institute for Immunology, CH-4001 Basel, Switzerland; 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