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. 2022 Mar 3;24(4):415–423. doi: 10.1007/s12017-022-08705-2

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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/.

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Fig. 1 — GF23-2D2 mice spontaneously developed myelitis and ataxia. A–C GF23-2D2 mice spontaneously developed a myelitis and ataxia, whereas WT, 2D2 and GF-IL23 mice did not show any neurological deficits. D Consistent with the clinical phenotype, the GF23-2D2 mice showed significant weight loss compared with WT, 2D2, and GF-IL23 mice with *P < 0.05 and ***P < 0.001