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. 2019 Feb 7;10:633. doi: 10.1038/s41467-019-08328-5

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© The Author(s) 2019

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. 5 — RGM-A-dependent monocyte intracellular signaling. WT animals were exposed to ZyA induced peritonitis and treated with with RGM-A and/or β₂AR agonist or vehicle and peritoneal monocytes were collected 12 h after ZyA injection. a The NF-κB, b the mTOR, and c the PI3K/Akt signaling pathways were assessed in peritoneal monocytes by using a protein microarray. Samples were pooled from 3 to 4 mice in each group for each experiment. d Schematic model of the interaction and synergistic effect of sympathetic nervous system and RGM-A