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. 2019 Nov 4;9:15932. doi: 10.1038/s41598-019-52041-8

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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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Graphical synopsis. In injured tissue, circulating neutrophils (blue) are recruited to postcapillary venules, where they arrest on microvascular endothelial cells. Supported by hydrodynamic forces, circulating platelets (dark red) get in close contact with neutrophils and the endothelium. This enables platelets to form tethers anchoring to adherent neutrophils and endothelial cells, thus accelerating thrombus formation. In arterioles, neutrophils are not recruited to the vessel wall and platelet thrombus formation is not facilitated by these immune cells.