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Blood, 15 July 2005, Vol. 106, No. 2, pp. 584-592. Prepublished online as a Blood First Edition Paper on April 5, 2005; DOI 10.1182/blood-2004-12-4942. This Article Full Text Full Text (PDF) Supplemental Videos All Versions of this Article: 2004-12-4942v1 106/2/584    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Yang, L. Articles by Luscinskas, F. W. Search for Related Content PubMed PubMed Citation Articles by Yang, L. Articles by Luscinskas, F. W. Related Collections Hemostasis, Thrombosis, and Vascular Biology Immunobiology Phagocytes Cell Adhesion and Motility Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY ICAM-1 regulates neutrophil adhesion and transcellular migration of TNF--activated vascular endothelium under flow Lin Yang, Richard M. Froio, Tracey E. Sciuto, Ann M. Dvorak, Ronen Alon, and Francis W. Luscinskas From the Center for Excellence in Vascular Biology, Department of Pathology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA; the Departments of Pathology, Beth Israel-Deaconess Medical Center and Harvard Medical School, Boston, MA; and the Department of Immunology, The Weizmann Institute of Science, Rehovot, Israel. In vivo, leukocyte transendothelial migration (TEM) occurs at endothelial cell junctions (paracellular) and nonjunctional (transcellular) locations, whereas in vitro models report that TEM is mostly paracellular. The mechanisms that control the route of leukocyte TEM remain unknown. Here we tested the hypothesis that elevated intercellular adhesion molecule-1 (ICAM-1) expression regulates the location of polymorphonuclear leukocyte (PMN) TEM. We used an in vitro flow model of tumor necrosis factor- (TNF-)-activated human umbilical vein endothelium cells (HUVECs) or an HUVEC cell line transfected with ICAM-1GFP (green fluorescent protein) and live-cell fluorescence microscopy to quantify the location of PMN adhesion and TEM. We observed robust transcellular TEM with TNF--activated HUVECs and ICAM-1GFP immortalized HUVECS (iHUVECs). In contrast, primary CD3+ T lymphocytes exclusively used a paracellular route. Endothelial ICAM-1 was identified as essential for both paracellular and transcellular PMN transmigration, and interfering with ICAM-1 cytoplasmic tail function preferentially reduced transcellular TEM. We also found that ICAM-1 surface density and distribution as well as endothelial cell shape contributed to transcellular TEM. In summary, ICAM-1 promotes junctional and nonjunctional TEM across inflamed vascular endothelium via distinct cytoplasmic tail associations. (Blood. 2005;106:584-592) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Neutrophil migration across endothelium: transcellular or paracellular? Ke Zen and Charles A. Parkos Blood 2005 106: 394-395. [Full Text] [PDF] This article has been cited by other articles: M. Stefanidakis, G. Newton, W. Y. Lee, C. A. Parkos, and F. W. 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