Plasmodium falciparum picks (on) EPCR.
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.
The Center for Vascular Biology Research and.
William C
WC
Aird
Laurent O
LO
Mosnier
Rick M
RM
Fairhurst
D015703:Antigens, CD / Q000378:metabolism*; D001777:Blood Coagulation; D002448:Cell Adhesion; D000074283:Endothelial Protein C Receptor; D004730:Endothelium, Vascular / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism* / Q000469:parasitology*; D006801:Humans; D016779:Malaria, Cerebral / Q000097:blood / Q000378:metabolism* / Q000469:parasitology; D016778:Malaria, Falciparum / Q000097:blood / Q000378:metabolism* / Q000469:parasitology; D055806:Microvessels; D009928:Organ Specificity; D010963:Plasmodium falciparum / Q000235:genetics / Q000378:metabolism*; D011485:Protein Binding; D011956:Receptors, Cell Surface / Q000378:metabolism*
D015703:Antigens, CD; D000074283:Endothelial Protein C Receptor; C478370:PROCR protein, human; D011956:Receptors, Cell Surface