Abstract
This study examined the mechanisms of clearance of Plasmodium yoelii-infected erythrocytes (RBC) from the peripheral circulation of mice. Parasitized RBC labeled with 51Cr were cleared from the blood of normal C57BL/6 mice at a much more rapid rate than were nonparasitized RBC, and preincubation of parasitized RBC in antiplasmodial antibody failed to significantly enhance clearance. This apparent antibody-independent clearance mechanism was markedly abrogated by splenectomy, indicating a major role for the spleen in parasitized RBC clearance. Macrophage inactivation by silica treatment also impaired parasitized RBC clearance, but to a lesser extent than splenectomy. Although abrogation of phagocytic function by silica treatment had little effect on splenic sequestration of parasitized RBC, hepatic sequestration was significantly depressed. Schizont- and late trophozoite-infected RBC were rapidly removed from the circulation, whereas RBC containing rings and early trophozoites showed less clearance over time. These data are consistent with the hypothesis that the architecture of the spleen serves as a sieve to entrap RBC that contain malarial parasites, particularly the more mature developmental forms.