IFNG and autoimmune disease: However, the immunological phenotypes of IFN-γ deficiency and T-bet deficiency are distinct: reducing IFN-γ signaling in mice by using IFN-γ-deficient lines or blocking IFN-γ paradoxically worsens their susceptibility to autoimmune diseases (which are thought to be Th1/Th17 driven), most notably experimental allergic encephalomyelitis (EAE; Ferber et al., 1996).