SEARCH:   Advanced

Blood, 1 May 2006, Vol. 107, No. 9, pp. 3593-3599. Prepublished online as a Blood First Edition Paper on January 17, 2006; DOI 10.1182/blood-2005-09-3695. This Article Full Text Full Text (PDF) All Versions of this Article: 2005-09-3695v1 107/9/3593    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 Evans, B. J. Articles by Landis, R. C. Search for Related Content PubMed PubMed Citation Articles by Evans, B. J. Articles by Landis, R. C. Related Collections Cell Adhesion and Motility Signal Transduction Free Research Articles Hemostasis, Thrombosis, and Vascular Biology Immunobiology Phagocytes Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Shedding of lymphocyte function–associated antigen-1 (LFA-1) in a human inflammatory response Betsy J. Evans, Alison McDowall, Peter C. Taylor, Nancy Hogg, Dorian O. Haskard, and R. Clive Landis From the Eric Bywaters Centre for Vascular Inflammation, Faculty of Medicine, Imperial College London, Hammersmith Hospital, London, United Kingdom; the Leukocyte Adhesion Laboratory, Cancer Research UK, London, United Kingdom; and the Kennedy Institute for Rheumatology, Faculty of Medicine, Imperial College London, London, United Kingdom. Shedding of adhesion molecules has been described for members of the selectin and immunoglobulin superfamilies, but integrins are not known to be shed. Here, we describe shedding of the integrin lymphocyte function–associated antigen-1 (LFA-1; CD11a/CD18) from human leukocytes during the cutaneous inflammatory response to the blistering agent cantharidin. Expression of LFA-1 was significantly diminished on blister-infiltrated neutrophils (P < .001) and monocytes (P = .02) compared with cells in peripheral blood, but expression on lymphocytes remained unchanged. A capture enzyme-linked immunosorbent assay (ELISA) indicated that LFA-1 was shed into blister fluid as a heterodimer expressing an intact headpiece with I and I-like epitopes. However, a CD11a central region epitope, G25.2, was absent and this remained expressed as a "stub" on the cell surface of blister neutrophils. Western analysis of soluble LFA-1 revealed a truncated 110-kDa CD11a chain and a minimally truncated 86-kDa CD18 chain. However, LFA-1 was shed in a ligand-binding conformation, since it expressed KIM-127 and 24 activation epitopes and bound to solid-phase ICAM-1. Shed LFA-1 was also detected in a synovial effusion by ELISA and Western analysis. We hypothesize that LFA-1 shedding may play a role in leukocyte detachment after transendothelial migration and in regulating integrin-dependent outside-in signaling. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Shedding of heterodimeric leukocyte integrin Martin E. Hemler Blood 2006 107: 3417-3418. [Full Text] [PDF] This article has been cited by other articles: B.J. Evans, D.O. Haskard, J.R. Finch, I.R. Hambleton, R.C. Landis, and K.M. Taylor The inflammatory effect of cardiopulmonary bypass on leukocyte extravasation in vivo. J. Thorac. Cardiovasc. Surg., May 1, 2008; 135(5): 999 - 1006. [Abstract] [Full Text] [PDF] R. K. Andrews, D. Karunakaran, E. E. Gardiner, and M. C. Berndt Platelet Receptor Proteolysis: A Mechanism for Downregulating Platelet Reactivity Arterioscler. Thromb. Vasc. Biol., July 1, 2007; 27(7): 1511 - 1520. [Abstract] [Full Text] [PDF]

	Blood Online is supported in part by Genentech BioOncology and Biogen Idec
	Copyright © 2006 by American Society of Hematology         Online ISSN: 1528-0020