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Please use this identifier to cite or link to this item: http://repository.li.mahidol.ac.th/dspace/handle/123456789/22293
Title: Human vascular endothelial cell adhesion receptors for plasmoclium falciparum-infected erythrocytes: Roles for endothelial leukocyte adhesion molecule 1 and vascular cell adhesion molecule 1
Authors: Christian F. Ockenhouse
Tatsuya Tegoshi
Yoshimasa Maeno
Christopher Benjamin
May Ho
Khin Ei Kan
Ye Thway
Kyan Win
Masamichi Aikawa
Roy R. Lobb
Walter Reed National Military Medical Center
CASE School of Medicine
Biogen Inc.
Mahidol University
University of Calgary
Department of Medical Research
Military Hospital
Keywords: Immunology and Microbiology;Medicine
Issue Date: 1-Oct-1992
Citation: Journal of Experimental Medicine. Vol.176, No.4 (1992), 1183-1189
Abstract: The clinical complications associated with severe and cerebral malaria occur as a result of the intravascular mechanical obstruction of erythrocytes infected with the asexual stages of the parasite, Plasmodiumfakiparum. We now report that a primary P.fakiparum-infected erythrocyte (parasitized red blood cell [PRBC]) isolate from a patient with severe complicated malaria binds to cytokineinduced human vascular endothelial cells, and that this adhesion is in part mediated by endothelial leukocyte adhesion molecule 1 (ELAM-1) and vascular cell adhesion molecule 1 (VCAM-1). PRBC binding to tumor necrosis factor α (TNF-α-activated human vascular endothelial cells is partially inhibited by antibodies to ELAM-1 and ICAM-1 and the inhibitory effects of these antibodies is additive. PRBCs selected in vitro by sequential panning on purified adhesion molecules bind concurrently to recombinant soluble ELAM-1 and VCAM-1, and to two previously identified endothelial cell receptors for PRBCs, ICAM-1, and CD36. Post-mortem brain tissue from patients who died from cerebral malaria expressed multiple cell adhesion molecules including ELAM-1 and VCAM-1 on cerebral microvascular endothelium not expressed in brains of individuals who died from other causes. These results ascribe novel pathological functions for both ELAM-1 and VCAM-1 and may help delineate alternative adhesion pathways PRBCs use to modify malaria pathology. © 1992, Rockefeller University Press., All rights reserved.
URI: https://www.scopus.com/inward/record.uri?partnerID=HzOxMe3b&scp=0026759659&origin=inward
http://repository.li.mahidol.ac.th/dspace/handle/123456789/22293
ISSN: 15409538
00221007
Appears in Collections:Scopus 1991-2000

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