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The mechanism of development of host resistance to blood-stage malarial infection was studied by use of an irradiation-induced attenuated variant, Plasmodium berghei XAT, obtained from a lethal strain, P. berghei NK65. The infection enhanced mRNA expression of interleukin (IL)-12 p40 and also of interferon (IFN)-gamma, IL-4, IL-10, and cytokine-inducible nitric oxide synthase (iNOS) in spleen. Treatment of these mice with anti-IL-12 or anti-IFN-gamma led to the progression of parasitemia and fatal outcome. Anti-IL-12 treatment significantly reduced the secretion and mRNA expression of IFN-gamma and greatly diminished the augmentation of iNOS mRNA expression. In addition, recombinant IL-12 administration delayed the onset of parasitemia because of the enhanced IFN-gamma production. These results suggest that blood-stage P. berghei XAT infection induces IL-12 production, which is important for the development of host resistance via IFN-gamma production.

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

Interleukin‐12‐Dependent Mechanisms in the Clearance of Blood‐Stage Murine Malaria Parasite<i>Plasmodium berghei</i>XAT, an Attenuated Variant of<i>P. berghei</i>NK65

Interleukin‐12‐Dependent Mechanisms in the Clearance of Blood‐Stage Murine Malaria ParasitePlasmodium bergheiXAT, an Attenuated Variant ofP. bergheiNK65