a–c, EAE was induced in control (WT), GfapcreAhrfl/fl (GFAP-AHR), or CX3CR1-AHR EAE mice. Starting from day 7, mice were injected daily intraperitoneally with indoxyl-3-sulfate (I3S), given a tryptophan-depleted diet (TDD), or kept on a control diet. Clinical course of EAE mice under treatment conditions as indicated. Representative of two independent experiments with n = 4 mice per group. d–f, EAE was induced in wild-type mice, which were treated with lentiviruses to knockdown AHR in astrocytes (pGFAP-shAhr) or microglia (pCD11b-shAhr). A noncoding RNA was used as a control. Flow cytometry quantification of AHR expression in astrocytes and microglia by FACS. d, Representative histograms of n = 4 mice per group. Numbers indicate percentage of AHR-positive cells; thin lines denote isotype control, thick lines denote AHR staining. e, Quantification of AHR-positive astrocytes and microglia as in d. Representative of two independent experiments with four biological replicates. f, EAE mice with knock down of AHR in astrocytes, microglia, or both as in d were subjected to daily I3S injections, TDD, or control diet conditions starting on day 14 after disease induction. Clinical course of n = 4 mice per group. Representative of two independent experiments with n = 4 mice per group. g, Quantification of CNS-infiltrating pro-inflammatory monocytes as determined by FACS at day 28 of EAE. Representative of two independent experiments with three biological replicates. Data are mean ± s.e.m. P values were determined by two-way ANOVA (a, f), or one way ANOVA followed by Tukey’s post-hoc test (e, g).