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. 2021 Feb 26;11:4735. doi: 10.1038/s41598-021-84023-0

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© The Author(s) 2021

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 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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Graphical representation of cellular and molecular mechanisms of the protective effect of CpG-pre-pDCs against EAE. Upon adoptive transfer of pDC progenitors at d-12, the onset of clinical signs, TGF-β released only by CpG-pre-pDCs in the first 3 days in the spinal cord (light blue zone) of mice protects against EAE by prompting host pDCs to release in turn TGF-β and promoting accumulation of CD11c⁺CD11b⁺ cDCs and IL-10⁺ B cells. CpG-pre-pDCs, once migrated to the spinal cord, additionally release IL-27 that from day-22 onwards, ensures late protection against EAE. BBB blood brain barrier. The figure was created using Biorender.com.