In health, Treg and Th17-cell ability to upregulate CD39 upon exposure to AHR endogenous and exogenous ligands, results from effective interactions between AHR and ARNT. In AIH Treg and Th17-cells, increase in the levels of the AHR inhibitors AHRR (Treg) and HIF-1α (Th17) results in altered AHR signalling and consequent inability to effectively upregulate CD39. In AIH Treg, AHR signalling is further impacted because of heightened expression of the AHR non-canonical binding partner Erα, the expression of which directly correlates with steroid dose.