Plasmodium chabaudi adami: interferon-γ but not IL-2 is essential for the expression of cell-mediated immunity against blood-stage parasites in mice

γδ T Cells but Not NK Cells Are Essential for Cell-Mediated Immunity against Plasmodium chabaudi Malaria

“…The critical role of IFN-␥ in immunity to malaria is uncontested. The neutralization of IFN-␥ by MAb in WT mice or depression of IFN-␥ production in KO mice prolongs the duration of P. chabaudi parasitemia, which eventually cures (39,46), but in J H Ϫ/Ϫ mice leads to high levels of noncuring parasitemia (1,46). These data indicate that IFN-␥ plays an important role in AMI immunity to malaria and an essential role in CMI to the parasite.…”

“…P. chabaudi malaria is more severe in WT mice treated with neutralizing antibody and in IFN-␥ Ϫ/Ϫ mice, as indicated by the increased magnitude and duration of parasitemia and mortality in mice deficient in IFN-␥ versus intact controls (24,39,46). In B-cell-deficient animals, the similar neutralization of IFN-␥ by treatment with anti-IFN-␥ monoclonal antibody (MAb) or gene knockout of IFN-␥ has an even greater effect on the time course of parasitemia, which remains at high levels and fails to cure (1,46), indicating that IFN-␥ is essential for the expression of antiparasite CMI and contributes to AMI in this model system.…”

Splenic γδ T Cells Regulated by CD4+T Cells Are Required To Control ChronicPlasmodium chabaudiMalaria in the B-Cell-Deficient Mouse

“…Whether similar mechanisms function in vivo remains to be determined. Both CD4 ϩ T cells and ␥␦ T cells from chronically infected mice expressed mRNA for IFN-␥, which plays an important role in AMI to P. chabaudi malaria and an essential role in CMI to blood-stage infection (1,37,48). When J H Ϫ/Ϫ mice are made IFN-␥ deficient by treatment with neutralizing MAb or gene-targeted knockout, they develop noncuring high-grade parasitemia despite having the same numbers of B220 ϩ splenic ␥␦ T cells as infected J H Ϫ/Ϫ single-knockout mice (unpublished observations).…”

Suppression of LethalPlasmodium yoeliiMalaria following Protective Immunization Requires Antibody-, IL-4-, and IFN-γ-Dependent Responses Induced by Vaccination and/or Challenge Infection

“…In naive mice, IFN-␥ has been shown to be essential for immunity to blood-stage P. yoelii (31,32,36,61) and P. chabaudi (61)(62)(63) parasites. In P. yoelii, a lack of IFN-␥ early during P. yoelii malaria has been correlated with disease progression and lethality (32,36).…”