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Toxoplasmic encephalitis is an AIDS-defining condition. The decline of IFN-γ-producing CD4 +  T cells in AIDS is a major contributing factor in reactivation of quiescent  Toxoplasma gondii  to an actively replicating stage of infection. Hence, it is important to characterize CD4-independent mechanisms that constrain acute  T. gondii  infection. We investigated the in vivo regulation of IFN-γ production by CD8 +  T cells, DN T cells and NK cells in response to acute  T. gondii  infection. Our data show that processing of IFN-γ by these non-CD4 cells is dependent on both IL-12 and IL-18 and the secretion of bioactive IL-18 in response to  T. gondii  requires the sensing of viable parasites by multiple redundant inflammasome sensors in multiple hematopoietic cell types. Importantly, our results show that expansion of CD8 +  T cells, DN T cells and NK cell by S4B6 IL-2 complex pre-treatment increases survival rates of mice infected with  T. gondii  and this is dependent on IL-12, IL-18 and IFN-γ. Increased survival is accompanied by reduced pathology but is independent of expansion of T Reg  cells or parasite burden. This provides evidence for a protective role of IL2C-mediated expansion of non-CD4 cells and may represent a promising lead to adjunct therapy for acute toxoplasmosis.

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Treatment of mice with S4B6 IL-2 complex prevents lethal toxoplasmosis via IL-12- and IL-18-dependent interferon-gamma production by non-CD4 immune cells