The study investigates the late developmental plasticity of T helper 17 (Th17) cells, which are crucial in both host protection and autoinflammatory disorders. Th17 cells are characterized by the production of interleukin (IL)-17A and IL-17F, and their development is independent of the Th1 pathway. However, mice deficient in STAT4 and T-bet, two key transcription factors, are protected from autoimmunity associated with Th17 pathogenesis. To explore the fate and pathogenic potential of Th17 cells and the origin of interferon (IFN)-γ-producing T cells during Th17 immunity, researchers developed IL-17F reporter mice to identify cells committed to expressing IL-17F and IL-17A. They found that Th17 cells require TGF-β for sustained expression of IL-17F and IL-17A. In the absence of TGF-β, both IL-23 and IL-12 act to suppress IL-17 and enhance IFN-γ production in a STAT4- and T-bet-dependent manner, though with distinct efficiencies. These findings support a model of late Th17 developmental plasticity, which has implications for autoimmunity and host defense. The study also highlights the role of STAT4 and T-bet in the conversion of Th17 cells to IFN-γ-producing cells, and the importance of IL-12 in driving this transition. Additionally, the research demonstrates that Th17 cells induced by TGF-β and IL-6 can induce colitis upon transfer into immunodeficient recipients, and that the emergence of IFN-γ-producing cells from Th17 precursors is a significant component of the effector T cell response during immunopathology.The study investigates the late developmental plasticity of T helper 17 (Th17) cells, which are crucial in both host protection and autoinflammatory disorders. Th17 cells are characterized by the production of interleukin (IL)-17A and IL-17F, and their development is independent of the Th1 pathway. However, mice deficient in STAT4 and T-bet, two key transcription factors, are protected from autoimmunity associated with Th17 pathogenesis. To explore the fate and pathogenic potential of Th17 cells and the origin of interferon (IFN)-γ-producing T cells during Th17 immunity, researchers developed IL-17F reporter mice to identify cells committed to expressing IL-17F and IL-17A. They found that Th17 cells require TGF-β for sustained expression of IL-17F and IL-17A. In the absence of TGF-β, both IL-23 and IL-12 act to suppress IL-17 and enhance IFN-γ production in a STAT4- and T-bet-dependent manner, though with distinct efficiencies. These findings support a model of late Th17 developmental plasticity, which has implications for autoimmunity and host defense. The study also highlights the role of STAT4 and T-bet in the conversion of Th17 cells to IFN-γ-producing cells, and the importance of IL-12 in driving this transition. Additionally, the research demonstrates that Th17 cells induced by TGF-β and IL-6 can induce colitis upon transfer into immunodeficient recipients, and that the emergence of IFN-γ-producing cells from Th17 precursors is a significant component of the effector T cell response during immunopathology.