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. 2020 Mar 9;11:1253. doi: 10.1038/s41467-020-15088-0

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© The Author(s) 2020

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. 7 — a APC and HDL, the ligand of EPCR and SR-BI, respectively, suppress expression of adhesion molecules in activated endothelial cells. APC also negatively regulates the differentiation of CD4+ T cells expressing EPCR into Th17 cells, and thus inhibits the production of Th17-related cytokines, including IL-17A, IL-17F, IL-21, and IL-22. These mechanisms contribute to the resolution of vascular inflammation in normal condition. b Autoantibodies against EPCR or SR-BI block bindings of corresponding ligands to their receptors, which promote expression of adhesion molecules in endothelial cells. In addition, anti-EPCR autoantibodies disrupt the negative regulation of Th17 differentiation by APC and thus amplify Th17-mediated immune response. As a result, autoantibodies in TAK inhibit the spontaneous resolution of activated immune responses in the vessel wall and thus lead to the chronic vascular inflammation.