IFNG and experimental autoimmune encephalomyelitis: For example, although Th1 cells and their signature cytokine IFN-γ are demonstrated to be pathogenic in EAU [13], innate IFN-γ from natural killer (NK) cells and natural killer T (NKT) cells are protective, as systemic depletion of IFN-γ exacerbates the disease development, in association with elevated Th17 response, in EAU [14,15] and experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis [16].