Susceptibility to inflammation in GILZ-KO mice was exacerbated in chemically induced Th1-type colitis; GC treatment increased the Treg number and functions and alleviated the symptoms of colitis in WT mice but not in GILZ-deficient mice, suggesting that the immunosuppressive properties of GC depend, at least in part, on GILZ and involve the modulation of Treg function in vivo. Here, TSC22D3 is linked to colitis.