IFNG and experimental autoimmune encephalomyelitis: For example, experimental autoimmune encephalomyelitis (EAE) and collagen-induced arthritis (CIA) have been historically associated with IFN-γ-producing Th1-dominant responses 1, but mice deficient in IFN-γ or IFN-γ receptor develop EAE at an accelerated rate 2–4 and, similarly, deficiency in IFN-γ or IFN-γ receptor leads to more severe CIA and the development of CIA in otherwise non-susceptible strains 5–7.