Little is known of the mechanisms whereby antibody can transfer protective immunity to malaria. We therefore examined in vivo the effects of the administration of hyperimmune serum to nonimmune rats on 1) the course of parasitemia after inoculation of P. berghei-infected erythrocytes, 2) the clearance of 51Cr-labeled infected erythrocytes, 3) the intraerythrocytic maturation of parasites, and 4) the invasion of erythrocytes by merozoites. Parasitemia rose in rats treated with normal serum but decreased in rats treated with hyperimmune serum. This protective effect of hyperimmune serum was not associated with a significant increase in the rate of clearance or the total reticuloendothelial organ uptake of 51Cr-labeled infected erythrocytes. Hyperimmune serum had no effect on the early intraerythrocytic development of the parasites since parasite maturation from ring form to trophozoite stage progressed normally. However, ring forms failed to increase after schizont rupture in recipients of hyperimmune serum, whereas an increase was observed in recipients of normal serum. Our in vivo study therefore supports in vitro evidence that the major protective role of antibody is to interfere with the interaction of the extracellular form of the parasite (merozoite) and the erythrocyte during the invasion process. Specifically, our data exclude opsonization of infected erythrocytes or interference with early parasite maturation as major mechanisms of antibody-mediated protection. Finally, our study suggests that the spleen may play an additional role by removing opsonized merozoites, since hyperimmune serum administered to splenectomized rats was only partially effective in preventing merozoite invasion of erythrocytes.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Immunology|
|State||Published - Dec 1 1979|
ASJC Scopus subject areas
- Immunology and Allergy