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. 2022 May 12;5:449. doi: 10.1038/s42003-022-03376-y

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© The Author(s) 2022

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — MIP was induced in Ncf1-deficient mice with or without co-administration of 1,3-β-glucan (a, b) or 1,6-β-glucan (c, d). Arthritis severity was followed, and spleen weight measured at the end of the experiment at day 8 in (a, b) and day 7 in (c, d). MIP was induced in Ncf1-deficient mice on day 0, and 3 mg of 1,6-β-glucan administered one day later (e). Arthritis severity was followed, and spleens weighted at the end of the experiment on day 9. The number of mice in each group is shown in parentheses. The data in (c) are pooled from two experiments, except the doses of 1 mg and 2 mg which were included only in one experiment. Spleen index was calculated with the data from one experiment. For groups with 1,6-β-glucan alone, N = 8 for arthritis, and N = 4 for spleen weight. Results are presented as mean and error bars represent the SEM. Statistical analyses were performed by Mann–Whitney test and * indicates a comparison between mannan and mannan + 3 mg β-glucan, whereas ^ indicates comparison between mannan and β-glucan in severity graphs. */^P < 0.05; **/^^P < 0.01; and ***P < 0.001.