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. 2023 Oct 4;21:364. doi: 10.1186/s12951-023-02089-6

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© The Author(s) 2023, corrected publication 2023

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/. 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. 1 — BSCBS and TJs were destroyed, and Treg cell infiltration increased after spinal cord injury. A, B The distribution and quantification of blood vessels labeled with CD31 (n = 3). C, D Fluorescence intensity and quantification of FITC-dextran around CD31-labeled blood vessels on day 7 after spinal cord injury (n = 4). E–H co-immunostaining and quantification of TJS-related proteins and vascular at injury sites and adjacent sites on day 7 after spinal cord injury (arrows: intact blood vessels; triangles: damaged blood vessels) (n = 3). I Western blotting detected the expression of TJs protein at each time point after spinal cord injury. J, K Representative staining and quantification of Foxp3-labeled Treg cells at the injured site after spinal cord injury (n = 3)