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Levamisole Inhibits Sequestration of Infected Red Blood Cells in Patients with Falciparum Malaria
Author(s) -
Arjen M. Dondorp,
Kamolrat Silamut,
Prakaykaew Charunwatthana,
Sunee Chuasuwanchai,
Ronnatrai Ruangveerayut,
Somyot Krintratun,
Nicholas J. White,
May Ho,
Nicholas Day
Publication year - 2007
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/519287
Subject(s) - parasitemia , plasmodium falciparum , biology , malaria , quinine , immunology , levamisole , cd36 , pharmacology , receptor , biochemistry
Sequestration of infected red blood cells (iRBCs) in the microcirculation is central to the pathophysiology of falciparum malaria. It is caused by cytoadhesion of iRBCs to vascular endothelium, mediated through the binding of Plasmodium falciparum erythrocyte membrane protein-1 to several endothelial receptors. Binding to CD36, the major vascular receptor, is stabilized through dephosphorylation of CD36 by an alkaline phosphatase. This is inhibited by the alkaline phosphatase-inhibitor levamisole, resulting in decreased cytoadhesion.

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