Fig. 3

Physiological effects of AhR in the gastro-intestinal tract. AhR ligands can be generated from the diet and/or microbiota and are able to activate AhR. In the intestine, AhR is expressed by intestinal epithelial cells (IEC), where it is involved in epithelial cell renewal and turn over. IECs have a role in the regulation of AhR ligand availability to intestinal immune cells, including antigen presenting cells (APCs), innate lymphoid cells (ILCs), Th17/Th22 cells, and intraepithelial lymphocyte γδ T cells (γδ T cells). All of these immune cells express AhR and its signaling is pivotal in the regulation of mucosal intestinal immune responses. Indeed, AhR is essential for the development and function of APCs. IL-23 is produced by APC in an AhR-independent manner but its effect on IL-22 production by ILC, Th17/Th22 and γδ T is mediated by AhR and RORγt. IL-22 is involved in mucosal wound-healing and it mediates innate antimicrobial resistance by inducing production of antimicrobial peptides (AMPs) by intestinal IECs. AhR is important for the development, maintenance, and function of ILC and γδ T cells, which have immune defense function. AhR is also essential for the function of Th22 and Th17 cells. Beyond its inflammatory pathology connotation, Th17 cells are important drivers of health, especially as they provide barrier protection and are involved in pathogen defense