Early Interactions Between Blood-Stage Plasmodium Parasites and the Immune System

Immunomodulatory effects of recombinant BCG expressing MSP-1C ofPlasmodium falciparumon LPS- or LPS+IFN-γ-stimulated J774A.1 cells

“…A strong innate immune response is important in early bloodstage malaria infection to prevent the parasite from entering human red blood cells and cause disease, while strong adaptive immune responses may protect against malaria by inhibiting merozoite invasion of erythrocytes as well as enhance clearance of infected erythrocytes from the circulation. 53,54 The mechanism by which rBCG induces more inflammatory response than parental BCG and LPS is not yet known. A previous report showed that glycosylphosphatidylinositol (GPI) anchors of merozoite membrane proteins released from rupturing malaria-infected erythrocytes capable to induce low levels of TNF-α production in macrophages.…”

Macrophage-Mediated but Gamma Interferon-Independent Innate Immune Responses Control the Primary Wave ofPlasmodium yoeliiParasitemia

“…Given the overwhelming evidence for a crucial role for IFN-␥ in controlling acute murine malaria infections (23,25,54), we considered the possibility that failure to produce IFN-␥ in the initial few days of lethal P. yoelii infection might explain the very rapid parasite growth. In apparent support of this possibility, and consistent with patterns of NK activation, an early burst of IFN-␥ was observed in the plasma of PyNL-infected (but not PyL-infected) mice on day 1 p.i.…”

“…Proinflammatory cytokines are essential for the control of intraerythrocytic Plasmodium infections in humans and in experimental animals (23,25,54). Antigen-presenting cells (APCs) produce interleukin 12 (IL-12), IL-15, IL-18, and tumor necrosis factor alpha (TNF-␣) (17,26,31,32,37,38,40,44,45,48), which can rapidly activate cells of the innate immune system to produce gamma interferon (IFN-␥) (31,32,44,64).…”

Cellulesnatural killeret immunité innée contre le paludisme

“…Cette activation serait importante pour aider à la production d'IFN-γ par les cellules Tγδ [32]. Une autre étude a montré que, in vitro, les Pf-E étaient également responsables d'une modulation négative de l'activation de DC dérivées de monocytes [33]. Cette modulation néga-tive, dépendante d'une interaction avec le récepteur CD36, se traduit par une absence d'expression des molécules du CMH, des molécules d'adhésion et de costimulation, ainsi qu'une absence de production d'IL-12 normalement observée en présence de LPS (lipopolysaccharide).…”