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Blood, 15 June 2006, Vol. 107, No. 12, pp. 4721-4727. Prepublished online as a Blood First Edition Paper on February 9, 2006; DOI 10.1182/blood-2005-11-4683. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-11-4683v1 107/12/4721    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 Huang, M.-T. Articles by Nourshargh, S. Search for Related Content PubMed PubMed Citation Articles by Huang, M.-T. Articles by Nourshargh, S. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Free Research Articles Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY ICAM-2 mediates neutrophil transmigration in vivo: evidence for stimulus specificity and a role in PECAM-1–independent transmigration Miao-Tzu Huang, Karen Y. Larbi, Christoph Scheiermann, Abigail Woodfin, Nicole Gerwin, Dorian O. Haskard, and Sussan Nourshargh From the Cardiovascular Medicine Unit, National Heart & Lung Institute, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom; and DG Thrombotic/Degenerative Joint Diseases, Aventis Pharma Deutschland, Frankfurt am Main, Germany. ICAM-2 has been implicated in leukocyte transmigration in vitro, but there is little in vivo evidence to support this. To address this, neutrophil migration was investigated in ICAM-2–deficient mice (KO) and in wild-type (WT) mice treated with an anti–ICAM-2 blocking monoclonal antibody (mAb) (3C4). In a peritonitis model, IL-1–induced accumulation of neutrophils was significantly reduced in mice treated with 3C4 (51% inhibition) and in KO mice (41% inhibition). In contrast, TNF-– or thioglycolate-induced responses were not suppressed in KO mice. Analysis of IL-1–induced leukocyte responses in cremasteric venules of KO animals by intravital microscopy indicated a defect in transmigration (44% inhibition) but not rolling or adhesion. As found before, TNF-–induced leukocyte transmigration was unaltered in the KO mice. WT mice treated with the anti–ICAM-2 mAb also exhibited a selective reduction in leukocyte transmigration in response to IL-1 while an anti–ICAM-1 mAb inhibited both leukocyte adhesion and transmigration. Interestingly, mAb 3C4 significantly suppressed IL-1–induced neutrophil transmigration in PE-CAM-1 KO animals in the peritonitis model but not in the cremaster muscle. The findings provide direct evidence for the involvement of ICAM-2 in neutrophil transmigration in vivo, though this role appears to be stimulus specific. Furthermore, ICAM-2 appears capable of mediating PECAM-1–independent leukocyte transmigration. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: ICAM-2 and PECAM-1: 2 steps in leukocyte transmigration Dietmar Vestweber Blood 2006 107: 4579-4580. [Full Text] [PDF] This article has been cited by other articles: E. J.A. van Wanrooij, P. de Vos, M. G. Bixel, D. Vestweber, T. J.C. van Berkel, and J. Kuiper Vaccination against CD99 inhibits atherogenesis in low-density lipoprotein receptor-deficient mice Cardiovasc Res, June 1, 2008; 78(3): 590 - 596. [Abstract] [Full Text] [PDF] B. Petri, M. 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Corada, M.-B. Voisin, C. Scheiermann, D. O. Haskard, E. Dejana, F. Krombach, and S. Nourshargh JAM-A mediates neutrophil transmigration in a stimulus-specific manner in vivo: evidence for sequential roles for JAM-A and PECAM-1 in neutrophil transmigration Blood, September 15, 2007; 110(6): 1848 - 1856. [Abstract] [Full Text] [PDF] J. D. van Buul, E. Kanters, and P. L. Hordijk Endothelial Signaling by Ig-Like Cell Adhesion Molecules Arterioscler. Thromb. Vasc. Biol., September 1, 2007; 27(9): 1870 - 1876. [Abstract] [Full Text] [PDF] M. G. Bixel, B. Petri, A. G. Khandoga, A. Khandoga, K. Wolburg-Buchholz, H. Wolburg, S. Marz, F. Krombach, and D. Vestweber A CD99-related antigen on endothelial cells mediates neutrophil but not lymphocyte extravasation in vivo Blood, June 15, 2007; 109(12): 5327 - 5336. [Abstract] [Full Text] [PDF] S. Nourshargh, F. Krombach, and E. Dejana The role of JAM-A and PECAM-1 in modulating leukocyte infiltration in inflamed and ischemic tissues J. Leukoc. Biol., October 1, 2006; 80(4): 714 - 718. [Abstract] [Full Text] [PDF] F. Wegmann, B. Petri, A. G. Khandoga, C. Moser, A. Khandoga, S. Volkery, H. Li, I. Nasdala, O. Brandau, R. Fassler, et al. ESAM supports neutrophil extravasation, activation of Rho, and VEGF-induced vascular permeability J. Exp. Med., July 10, 2006; 203(7): 1671 - 1677. [Abstract] [Full Text] [PDF]

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