IFNG and malaria: If induction of a Th17 response may, therefore, indirectly impair host ability to contain malaria through suppression of macrophage activities, the IFN-γ dominant response elicited by VL may partially compensate for this deficiency and act as a pre-priming stimulus upon Plasmodium infection, for the development of malaria adaptive immunity (via NKT cells, e.g.)and the nitric oxygen-dependent suppression of intra-hepatocytic forms.