First evidence came from a study by Monticelli and colleagues: Using an acute model of DSS-induced colitis, they could show AREG-derived from IL-33-activated ILC2s to be sufficient for the induction of goblet cell hyperplasia and expression of the mucin Muc2. Since this goblet cell activation was accompanied by a decreased overall disease severity of DSS-treated mice (69), this indicates that the protective effect of ILC2s on experimental colitis could be partially mediated by AREG-induced mucus production by goblet cells. Here, IL33 is linked to colitis.