They observed that in the experimental acute infection with T. cruzi, disabled mice in IL-17 presented a higher mortality rate and parasitemia when compared to the group control (C57BL/6, wild type), as well as a lower expression of cytokines, as IFN-γ, IL-6, and TNF-α, suggesting a protective role of IL-17 in the acute phase of the disease. This evidence concerns the gene IFNG and parasitic infectious disease.