CD36 and malaria: friends or foes?

Past research efforts examining the adhesive characteristics of Plasmodium falciparum-infected erythrocytes have focused primarily on sequestration in the peripheral circulation. Recent work has begun to elucidate how these adhesive phenotypes can also modulate host response to infection and how host-parasite interactions might be exploited to improve disease outcome. One example is the complex interaction that exists between the host scavenger receptor CD36 and P. falciparum. CD36 is not only involved in the sequestration of the parasite, but could also play a role in the innate and acquired immune response to infection. Recent work concerning the role of CD36 in sequestration and phagocytosis of infected erythrocytes, and in the modulation of dendritic cell and macrophage function by infected erythrocytes is reviewed here. The hypothesis that P. falciparum has evolved methods to inhibit immune and inflammatory responses that are harmful to both the parasite and the host is also explored.