IFNG and arthritic joint disease: [26]). For example, in the mouse model of multiple sclerosis, in vivo neutralization of IFN-γ resulted in exaggerated immune response and central nervous system immunopathology [27]. Similarly, in a mouse model of inflammatory bowel disease, IFN-γ has been shown to have anti-inflammatory role by suppressing IL-23 [28]. Collagen-induced arthritis is also exaggerated in the absence of IFN-γ signaling [29]. However, in the murine endotoxic shock model, IFN-γ seems to play a pathogenic role [30]. Similarly, IFN-γ has been shown to be lethal in lipopolysaccharide-sensitization models of TSS [31].