IFNG and colitis: Although in the present study, we primarily aimed to assess the precise impact of IFNγ rather than IL17 on the development of colitis in two separate mouse models, our results support the idea that IL17 compensates for the absence of T cell-derived IFNγ to drive colitis induction, suggesting that both the IFNγ- and IL17-mediated effects are targeted to attenuate chronic intestinal inflammation.