ABSTRACT
M alaria, due to infection with protozoan parasites of the genus Plasmodium, is a major cause of high morbidity and mortality worldwide, especially in sub-Saharan Africa. The multiplication of Plasmodium parasites in host red blood cells (RBC) during the asexual blood stage results in the severe symptoms associated with malaria, including ane mia, lactic acidosis and cerebral malaria. Immunity to blood stage malaria is complex and must be finely balanced to achieve protection of the host but prevent the development of pathology that is immunologically mediated. Innate and adaptive immune mechanisms are involved in protective immunity to Plasmodium parasites, and a network of proinflammatory cytokines, especially interferon (IFN)-y, and a variety of cell types including dendritic cells (DCs), natural killer (NK) cells, CD 4+ T cells and B cells as well as macrophages play important roles. These cell types act in concert to generate a type 1 antibody-dependent immune response, which mediates control o f parasite replication and clearance. The focus o f this review is how Plasmodium-wfected RBC interact with macrophages and other antigen presenting cells (APCs), such as DCs, and how such interactions affect the host immune response to Plasmodium infec tion and influence the outcome of malaria. Data are summarized from studies in humans and mice and evidence from both in vitro and in vivo studies are discussed. Information derived from studies on the interaction between Plasmodium parasites and macrophages will likely contribute to the development of an effective malaria vaccine and improved immunotherapies.
