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. 2021 Jun 28;18:145. doi: 10.1186/s12974-021-02193-0

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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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