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. 2022 Feb 2;19:27. doi: 10.1186/s12974-022-02386-1

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© The Author(s) 2022

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 — MaR1 attenuates inflammation in the spinal cord of mice undergoing EAE. A–G Graph showing the quantification of different immune cell populations in the spinal cord (A), the number of CD4 + T cells expressing IL-4, IL-10, IFNγ or IL-17A (B), the percentage of CD4 + T cells expressing the CD49b, FoxP3, tBet, GATA3 or RORγ (C), the percentage of regulatory lymphocytes expressing IL-10 (D), the percentage of macrophages expressing polarization markers (E), the ratio of Ly6C^low/Ly6C^high macrophages F and the percentage of microglial cells expressing polarization markers in the spinal cord after MaR1 or vehicle treatment. *p < 0.05; **p < 0.01; ***p < 0.001 vs. vehicle. Unpaired t-test (n = 4 per group). Data are shown as mean ± SEM