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. 2019 Jan 30;16:20. doi: 10.1186/s12974-019-1400-0

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© The Author(s). 2019

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 5 — Splenic sympathetic nerve-mediated anti-inflammatory pathway after stroke. After the acute stage of stroke, “brain-spleen cross-talk” not only inhibits the splenic inflammatory response by activating the SNS (reducing the production of inflammatory factors, such as TNF-α) [172] but also induces IL-10 production by lymphocytes in the spleen through activation of the NE-mediated PKA/cAMP pathway in other inflammatory-related disease models [174, 175]