Gut microbiota-derived metabolites and IL-22 signaling in inflammatory bowel disease: context-dependent regulation of mucosal repair and inflammation
It is proposed that the duration and magnitude of IL-22 exposure, its cellular source, the IL-22/IL-22BP balance, epithelial target-cell state, concurrent inflammatory signals, and disease context collectively determine whether IL-22 promotes mucosal repair or contributes to inflammatory amplification.