Attenuated Th1 differentiation accompanied by enhanced IFNγ-induced STAT1 phosphorylation.Favored Th1 and Th17 polarization following adoptive transfer in TCR transgenic mice and worsened aggressive colitis.Increased disease initiating Th1, Th17 and effector Treg dominant response in a mouse model of arthritis. This evidence concerns the gene STAT1 and arthritic joint disease.