Abstract
The accumulation of red blood cells (RBCs) parasitized by Plasmodium falciparum in many organs, particularly the brain and placenta, is probably the most extensively studied phenomenon in the pathogenesis of falciparum malaria. Parasitized RBCs (PRBCs) sequester as a result of receptor–ligand interactions between surface molecules on PRBCs and vascular endothelial cells or syncytiotrophoblasts of the placenta. Sequestration benefits the parasite, but can damage the host through microcirculatory obstruction and local or systemic inflammatory responses. The long-established view is that only RBCs infected with mature-stage parasites cytoadhere and sequester. In addition, the timing of the onset of the ability of PRBCs to adhere and their disappearance from the peripheral circulation correlates well with the expression of P. falciparum erythrocyte membrane protein-1 (PfEMP1), the molecule widely believed to be the major cytoadherence ligand on the PRBC surface.
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