Together with LTα, IL-22 stimulated the glycosylation of epithelial cells that is crucial for protection against S. Typhimurium186 infection and IL-22 and interferon λ jointly stimulated IL-1α release during Rotavirus infection.16,178,191 IL-22 production protected intestinal stem cells from damage caused by chemotherapy, irradiation or genotoxic stress by metabolites, such as toxic AHR ligands, which could in turn modulate IL-22 production.192–194. Here, IL1A is linked to Rotavirus infection.