ITE

Ki: 3 nM (AhR)

ITE is an endogenous agonist of AhR, binding directly to AHR, with a K _i of 3 nM. ITE (0.03-30 mg/mL) decreases the antigen-specific T-cell proliferative responses. ITE potently inhibits human pulmonary artery endothelial (HPAECs) growth at 10 and 20 µM, but shows no effect at 0.01-5 µM. ITE does not affect cell cycle progress of HPAECs at 10 and 20 µM, or induce expression of cleaved caspase-3 protein in HPAECs at 20 µM. In addition, ITE (20 µM) elevates CYP1A1 and CYP1B1 mRNA levels and decreases the levels of AhR protein in HPAECs.

ITE (200 μg, i.p.) significantly suppresses the development of experimental autoimmune uveitis (EAU) in mice. ITE reduces the proportions of cells expressing IFN-γ, IL-17, or IL-10 in mice. ITE also suppresses the secretion of inflammatory cytokines by LN cells in mice.