AHR and tuberculosis: Another study [15] has revealed how the TB pathogen Mtb exploits the host’s tryptophan metabolic pathway to delay T-cell immune responses: specifically, high levels of the tryptophan metabolite kynurenine were found to inhibit T-cell infiltration in the lungs of TB patients, whereas targeting the aryl hydrocarbon receptor (AhR) and indoleamine 2,3-dioxygenase 1 (IDO1) accelerated T-cell immune responses, thereby enhancing host control of Mtb infection.