In two key murine model systems of Th1-driven autoimmunity, collagen-induced arthritis (CIA) and experimental autoimmune encephalitis (EAE), it has been established that abrogation of IFN-γ signaling through monoclonal antibody therapy or genetic knockout produces a seemingly paradoxical increase in disease susceptibility and severity (13, 14). Here, IFNG is linked to Autoimmunity.