Spleen macrophages from Plasmodium berghei-infected mice are more efficient in the ingestion of parasitized reticulocytes than spleen macrophages obtained from normal animals. Other indications of spleen macrophage activation detected during malarial
infection are enhanced macrophage spreading and increased phagocytosis of opsonized and nonopsonized sheep erythrocytes (E). Peritoneal macrophages are not activated to a significant degree. The appearance of
antibodies directed against
Forssman antigen, but not to other erythrocyte
antigens, is also a feature of this
infection and explains the ingestion of unsensitized E by spleen macrophages of the diseased animals. The recognition and ingestion of parasitized reticulocytes by infected mice in mediated by cold-
agglutinin type
immunoglobulins that appear during P. berghei
infection and can be blocked by the Fc-
binding protein A from Staphylococcus aureus. In advanced stages of the disease, the serum of infected animals inhibits phagocytosis, probably because of the high level of circulating
immune complexes. Thus, the clearance of
malaria parasites is regulated by several elements of the immune system, in addition to levels of specific antimerozoite
antibodies, including the amount of
antibodies bound to reticulocytes, the presence of circulating
immune complexes, and the degree of macrophage stimulation.