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. 2019 Dec 3;10:2824. doi: 10.3389/fimmu.2019.02824

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Copyright © 2019 Granger, Peyneau, Chollet-Martin and de Chaisemartin.

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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Mechanisms of NET formation in autoimmunity. Autoantigen/IgG IC can bind to several FcγRs expressed at the neutrophil surface and induce their activation. In particular, NOX2 is activated and produce ROS that can in turn activate PAD4 leading to protein citrullination and chromatin decondensation. In parallel, ROS can also help MPO and NE degranulation and translocation to the nucleus contributing to chromatin unfolding. The nuclear membrane breaks down, the decondensed chromatin is released in the cytosol and becomes decorated with various cytosolic and granule-derived proteins. Finally, NETs are released exposing to the immune system a large number of autoantigens that can amplify this mechanism called lytic NETosis. In some conditions, in particular in SLE, these IC can also induce a non-lytic NOX2-independent NETosis via the production of mitochondria-derived ROS and/or DNA; in that case, neutrophils are still alive.