In fact, as opposed to their results obtained from IL-33 treatment in acute DSS colitis, Groβ et al. showed that IL-33 administration during repeated, chronic cycling of DSS caused a reduction of colitis, suppressed interferon gamma (IFNγ), and decreased bacterial translocation[44], supporting a protective role of IL-33 that the authors suggest may occur by switching from Th1- to Th2-driven immune responses. Here, IL33 is linked to colitis.