Plasmodium falciparum picks (on) EPCR-Reference-Cited by-同舟云学术

Plasmodium falciparum picks (on) EPCR

Published:2014-01-09 Issue:2 Volume:123 Page:163-167
ISSN:0006-4971
Container-title:Blood
language:en
Short-container-title:

Author:

Aird William C.¹²,Mosnier Laurent O.³,Fairhurst Rick M.⁴

Affiliation:

1. The Center for Vascular Biology Research and

2. Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA;

3. Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA; and

4. Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD

Abstract

Abstract Of all the outcomes of Plasmodium falciparum infection, the coma of cerebral malaria (CM) is particularly deadly. Malariologists have long wondered how some patients develop this organ-specific syndrome. Data from two recent publications support a novel mechanism of CM pathogenesis in which infected erythrocytes (IEs) express specific virulence proteins that mediate IE binding to the endothelial protein C receptor (EPCR). Malaria-associated depletion of EPCR, with subsequent impairment of the protein C system promotes a proinflammatory, procoagulant state in brain microvessels.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Link

http://ashpublications.org/blood/article-pdf/123/2/163/1376431/163.pdf

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