Central mediators of prototypical type 2 responses such as IL-33 are upregulated in the mucosa of patients with IBD, but how type 2 responses may drive pathological features of IBD or vitally contribute to the protective tissue response to damage still remains ill-defined. In this proposal, we aim to comprehensively address, how IL-33 production and signaling controls mutual interactions between the immune, stromal and epithelial cell compartments in vitro and in vivo. These insights together with the analysis of large cohorts of IBD patients and their stratification will be used to predict, whether targeting of type 2 molecules may be a strategy for personalized medicine in IBD.