IFNG and parasitic infectious disease: In contrast, IFN-γ−/− and IL12−/− mice succumbed soon after the end of treatment with intense parasitemia, parasitism and inflammatory processes [57] Furthermore, in TNFRp55−/− mice, the lack of signaling by this TNF-α receptor was unable to reduce microbicidal mechanisms related to the IFN-γ/NO axis in macrophages in vitro [58].