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. 2024 Aug 7;633(8029):433–441. doi: 10.1038/s41586-024-07803-4

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© The Author(s) 2024

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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Extended Data Fig. 10 — a–c. Flow cytometry analysis of blood from asymptomatic patients or stroke patients showing the percentage of monocytes (CD11b⁺), T cells (CD3⁺) and B cells (CD19⁺) out of total leukocytes (CD45⁺) (U test, asymptomatic patients, n = 7; symptomatic patients, n = 13). d. Representative immunoblot from asymptomatic and stroke patients for F. XIIa and β-actin (Quantification can be found in Fig. 4i). e. Quantification of MMP9 activity normalized to the activity in asymptomatic patients (Representative image shown in Fig. 4h). Raw membrane images of immunoblots with cropping indication can be found in Supplementary Fig. 1q. f. Overview schematic: Stroke leads to the release of NETosis-derived cell-free DNA activating the AIM2 inflammasome and subsequent secretion of IL-1β. The release of IL-1β drives MMP expression in atherosclerotic plaque, leading to fibrous cap destabilization. The fibrous cap rupture initiates the activation of the intrinsic coagulation cascade resulting in atherothrombosis and subsequent arterio-arterial embolism with secondary brain infarctions.