ILC3-derived IL-22 further triggers intestinal inflammation through detrimental neutrophil recruitment.330 The significantly reduced levels of IL-22 are associated with enhanced colonization resistance against S. typhimurium in mice.331 Similarly, in both a mouse model with intestinal fibrosis and patients with CD, the IL-23/IL-22 axis in the gut promotes intestinal fibrosis in a T cell- or B cell-independent manner. Here, IL22 is linked to Cowden disease.