Adherence of Plasmodium falciparum-infected erythrocytes (PRBCs) to the microvascular endothelium of specific organs and consequent sequestration is believed to be responsible for the development of malaria pathology. A number of studies have shown that cell adhesion molecules expressed on the surface of endothelial cells mediate the adherence. Recent studies indicate that a subpopulation of PRBCs adhere to chondroitin 4-sulfate (C4S). This adhesion can be effectively inhibited by C4S oligosaccharides. In pregnant women, the placenta specifically selects C4S-adherent PRBCs, and thus these phenotypes multiply and sequester in the intervillous spaces. Over successive pregnancies, women develop a protective humoral response to the C4S-adhesion phenotype. Disruption of C4S-mediated PRBCs adhesion using either a C4S oligosaccharide mimetic or an antiC4S-adhesion vaccine can be an efficient strategy for the treatment of malaria caused by C4S-adherent P. falciparum.
Research Article| August 01 1999
Adherence of Plasmodium falciparum-Infected Erythrocytes to Chondroitin 4-Sulfate
D. Channe Gowda;
Biosci Rep (1999) 19 (4): 261–271.
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D. Channe Gowda, Christian F. Ockenhouse; Adherence of Plasmodium falciparum-Infected Erythrocytes to Chondroitin 4-Sulfate. Biosci Rep 1 August 1999; 19 (4): 261–271. doi: https://doi.org/10.1023/A:1020542206916
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