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. 2021 Jul 20;7:52. doi: 10.1038/s41421-021-00280-3

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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 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. 6 — a A global view of the expression profiling of genes related to cell migration and adhesion in each cluster. The size of the dot corresponds to the percentage of cells expressing the gene in each cluster, and the color represents the average log normalized gene expression. Background heatmap shows the fold change in gene expression between each cluster and other clusters. Fold change was calculated using the function FindAllMarkers in R package Seurat with default parameters. Only positive markers (logFC > 0) in each cluster are shown in the heatmap. b Possible mechanism of cytotoxic T cells passing through the BBB in PD. Depiction of lymphocyte migration across endothelial cells was based on the leukocyte transendothelial migration pathway (KEGG pathway: hsa04670). During inflammation, adhesion molecules, chemokines and their receptors mediate the arrest, polarization, directed crawling and endothelial passage of lymphocytes on endothelial cells. Once T cells cross the BBB endothelium, T cells may recognize their cognate antigens and become reactivated behind the BBB. The amplified inflammatory response leads to parenchymal basement membrane damage. Finally, activated T cells enter the brain parenchyma to participate in central nervous system damage.