Fig. 7

Inactivation of the IDO1-aryl hydrocarbon receptor (AhR) pathway promotes neuroinflammation in Smek1 heterozygous mice. a AhR subcellular localization in spinal microglia detected by IBA1 and AhR costaining (scale bar, 25 μm). b Immunofluorescent staining of AhR in HMO6 cells treated with LPS (scale bar, 25 μm). c Correlation between IL-10 expression in the EAE brain and the clinical scores (r and p values are presented for wild-type and Smek1^-/+ mice data in the corresponding colors). The linearity of the correlation was tested with Pearson’s correlation. d, e Flow cytometry of the IL-10 level (d) and its quantification (e) in Th2 cells. Th2 cells were labeled with CD4 and IL-4. Data are presented as the mean ± SEM and were analyzed by the two-sided unpaired t test; *P < 0.05. f qPCR analysis of IL-10 in cultured mononuclear cells with and without treatment with LPS and anti-CD3&CD28. Data are presented as the mean ± SEM and were analyzed by the two-sided unpaired t test; *P < 0.05; ****P < 0.0001. g, h Mean MHC-II fluorescence intensity in the spleen (g) (n = 8 control, n = 6 Smek1^-/+) and lymph nodes (h) (n = 8 control, n = 6 Smek1^-/+). DCs were detected by labeling of CD11c and MHC-II. Data are presented as the mean ± SEM and were analyzed by the two-sided unpaired t test; *P < 0.05. i Schematic model of EAE pathogenesis in Smek1 heterozygotes