IFNG and systemic lupus erythematosus: Murine strains predisposed to developing lupus that are subsequently rendered homozygous for disruption of the IFNγ gene or treated with agents that deplete IFNγ have a longer life-span, a milder disease course, and far less renal damage than parental strains [17], [19] whereas infusions of exogenous IFNγ accelerated disease progression [23].