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. 2021 Nov 4;12:761946. doi: 10.3389/fimmu.2021.761946

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Copyright © 2021 Wu, Li, Tian, Ouyang, Ho, Alam and Li

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The detrimental effects of PAD2-mediated pyroptosis and ETosis during sepsis. PAD2 facilitates the activation of Caspase-11, a key regulator in non-canonical pyroptosis, and causes macrophage death. In addition, PAD2 can translocate into the nuclei of neutrophils or macrophages and citrullinate histone H3 to induce ETosis. CitH3 generated during this process may further activate the canonical pyroptotic pathway as a danger signal. aCaspase-1/11, activated Caspase-1/11; CitH3, Citrullinated histone H3; ETosis, cell death with release of extracellular traps (ETs); H3, Histone H3; HMGB1, high mobility group box 1; IL, interleukin; M/NETosis, neutrophil/macrophage death with release of extracellular traps; MPO, myeloperoxidase; NE, neutrophil elastase. Lines, pathways already known; Dotted lines, proposed hypothesis for the pathway to elucidated.