Fig. 1.

Functional differentiation of Treg cells into Th1-suppressing and Th1-like Tregs. FOXP3⁺ Tregs upregulate T-BET expression upon type I inflammatory stimuli such as IFNγ in a STAT1-dependent manner. T-BET⁺FOXP3⁺ Tregs retain their suppressive function and contribute to resolution of type I inflammation. Additional or subsequent exposure to IL-12 drives Tregs to express T-BET and release IFNγ. IFNγ-producing Tregs either contribute to resolution of type I inflammation (Th1-suppressing) or lose suppressive function and fail to efficiently control autoimmune responses (Th1-like Tregs)