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. 2022 Jan 3;19:1. doi: 10.1186/s12974-021-02372-z

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© The Author(s) 2021

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/. 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. 8 — A schematic diagram of SNHG15-based signaling circuit in stroke-induced immunosuppression. Activation of IL-4–JAK-STAT6 signaling pathway contributes to the expression of SNHG15, and SNHG15 uniquely inhibits the K63-linked ubiquitination of TRAF2, thereby attenuating inflammatory responses and promoting M2 macrophage polarization after stroke