IL-27R-/- mice infected with T. brucei efficiently controlled the first wave of parasitemia as infected wild-type did, but survived significantly shorter than infected wild-type mice (15 days vs. 32 days, p<0.01, Fig 8B), demonstrating an essential role of IL-27 signaling in prevention of the early mortality of mice infected with T. brucei. IL-27R-/- mice infected with T. brucei also showed enhanced IFN-γ production in plasma and supernatant fluids of spleen cultures, as well as enhanced serum activities of ALT, compared to infected wild-type mice (p<0.01 or <0.05, Fig 8C). The gene discussed is IFNG; the disease is parasitic infectious disease.