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.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, N.I.H., Intramural
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Review
MeSH terms
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Antigens, CD / metabolism*
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Blood Coagulation
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Cell Adhesion
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Endothelial Protein C Receptor
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Endothelium, Vascular / metabolism
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Erythrocytes / metabolism*
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Erythrocytes / parasitology*
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Humans
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Malaria, Cerebral / blood
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Malaria, Cerebral / metabolism*
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Malaria, Cerebral / parasitology
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Malaria, Falciparum / blood
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Malaria, Falciparum / metabolism*
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Malaria, Falciparum / parasitology
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Microvessels
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Organ Specificity
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Plasmodium falciparum / genetics
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Plasmodium falciparum / metabolism*
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Protein Binding
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Receptors, Cell Surface / metabolism*
Substances
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Antigens, CD
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Endothelial Protein C Receptor
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PROCR protein, human
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Receptors, Cell Surface