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. 2019 Feb 4;9:1283. doi: 10.1038/s41598-018-37852-5

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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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Schematic of overall findings. SLE- and RA-IgG displayed differential effects upon HC-neutrophils in our experiments. SLE-IgG enhanced both β₁ and β₂ integrin-mediated adhesion and also adhesion to endothelial cells. In contrast, RA-IgG only increased β₂ integrin-mediated adhesion. We observed higher levels of NETosis both in absence and presence of activated endothelial cells with the addition of SLE-IgG, whilst RA-IgG only enhanced NETosis in the absence of an endothelial monolayer.