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. 2022 Jul 22;12:12523. doi: 10.1038/s41598-022-15969-y

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© The Author(s) 2022

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Putative mechanism of anticardiolipin autoantibodies in COVID-19 severity. We hypothesize that SARS-CoV-2 infection of genetically-prone patients results in autoimmunity. Anticardiolipin autoantibodies (aCL) can bind a cell surface complex composed of lysobiphosphatidic acid (LBPA) and endothelial protein C receptor (EPCR). This interaction promotes cell death via reactive oxygen species (ROS). Then, releases extracellular DNA contributes to a heightened thrombo-inflammatory state associated with COVID-19 severity. The figure has been drawn by AB using InkScape 0.92, http://www.inkscape.org.