IFNG and systemic lupus erythematosus: Further support for the decisive role of IFNγ in murine lupus is demonstrated by the findings that depletion of IFNγ or IFNγ receptor in MRL-lpr and NZBWF1 mice reduced autoantibody production, improved histopathologic scores of kidneys, and promoted the survival of these lupus mice [25–27].