Concluding remarks
Research from the past few years has emphasized the crucial role of AHR signaling in several intestinal populations. While we now know that diverse T cell populations, as well as ILC3s rely on AHR ligand binding to develop, produce cytokines and/or remain at mucosal sites, more research is needed to determine how the vast array of AHR ligands have such disparate impacts on immune cell populations. Several factors likely affect the outcome of the interaction of an AHR ligand with the immune system: firstly, the origin of the ligand — is it an endogenous ligand, produced by the microbiota, a pathogen or a product of the diet? secondly, the concentration of the AHR ligand as well as its localization in the organism — is it present at similar concentrations throughout the intestine or is produced in particular areas? thirdly, how susceptible is the AHR ligand to degradation by enzymes like CYP1A1 — can it be metabolized into compounds with higher or lower affinity?
While the AHR pathway may be an attractive candidate to modify the intestinal immune response in order to control the overt inflammation characteristic of inflammatory bowel disease, more studies are needed to understand the nature of each AHR ligand so that we can identify specific ligands that render the desired effect.
