The role of CD36 in the pathophysiology of malaria: validation of a murine model and design of a clinical study

Abstract

CD36 has been shown to play a central role in phagocytic clearance of Plasmodium falciparum malaria, in cytoadherence of parasitized erythrocytes to endothelium and in maintaining a balanced cytokines state. Significant progress has been made in elucidating C1336-malaria interactions in vitro but an animal model of Plasmodium falciparum does not exist. We have developed and validated a murine malaria model for examining the in vivo role of CD36 in the pathophysiology of severe malaria infection. Accumulating evidence suggests that upregulation of CD36 may be beneficial in P. falciparum infections and may increase phagocytic clearance of P. falciparum malaria, modulate deleterious inflammatory responses to infection and decrease sequestration of malaria parasites in vital organs. This strategy may therefore represent a novel immunomodulatory treatment approach for severe P. falciparum malaria. We have designed a pilot human study to address this issue.