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. 2021 May 24;28(11):3125–3139. doi: 10.1038/s41418-021-00805-z

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© The Author(s) 2021

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. 2 — Pathways that regulate NET formation (see body text for references). Pattern recognizing receptors (PRR) initiate NADPH oxidase activation and a spike of cytosolic calcium activating neutrophil peptidylarginine deiminase 4 (PADI4) causing histone citrullination (yellow circle) and DNA decondensation. Chromatin and/or mitochondrial DNA is expelled and form NETs. Several necrotic cell death pathways may contribute to NETosis. Necroptosis involves RIPK1/RIPK3-mediated activation of MLKL and plasma membrane permeabilization contributing to the release of NETs. Pyroptosis involves canonical or non-canonical inflammasome activation by the caspases-1 or 4, respectively. Caspase-1 and 4 as well as NE cleave GSDMD and generates the N-GSDMD fragment with a pore-forming activity that enables the release of NETs. In addition, autophagic processes contribute to the release of NETs. Original illustration from the authors.