IL10 and colitis: Exogenous (e.g., β-naphthoflavone (β-NF) and TCDD) and candidate endogenous AhR ligands found in the gut (e.g., tryptophan (Trp) metabolites) have been shown to mediate protective pathways within murine models of colitis [5,6] and promote AhR-dependent anti-inflammatory signaling via Il-10/Il-10rα, tight junction formation, and enhanced barrier integrity within IECs [12].