The molecular basis for the cytoadherence of Plasmodium falciparum-infected erythrocytes to endothelium.
Human erythrocytes infected with the human malaria parasite Plasmodium falciparum, bind to post-capillary venular endothelium and to uninfected red blood cells via specific receptor-ligand interactions. The interactions between malaria-parasitized erythrocytes and host cells is a highly cooperative and finely regulated process which contributes both to the evasion of host immune mechanisms and to the pathogenesis of the disease, in particular the development of cerebral malaria. The cellular and molecular interactions responsible for the adhesion of parasitized red cells to host cells are the subject of this review.
Ockenhouse
C F
CF
Walter Reed Army Institute of Research, Walter Reed Army Medical Center, Washington DC.
D000818:Animals; D002448:Cell Adhesion; D015815:Cell Adhesion Molecules / Q000502:physiology; D004730:Endothelium, Vascular / Q000502:physiology*; D004912:Erythrocytes / Q000469:parasitology*; D006801:Humans; D016779:Malaria, Cerebral / Q000097:blood / Q000469:parasitology; D010963:Plasmodium falciparum / Q000502:physiology*; D016024:Receptors, Cytoadhesin / Q000502:physiology
D015815:Cell Adhesion Molecules; D016024:Receptors, Cytoadhesin