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. 2020 Jul 8;11(7):517. doi: 10.1038/s41419-020-2724-5

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© The Author(s) 2020

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. 4 — Generally, phagosomes become decorated with LC3 and are then trafficked to the lysosome for degradation (LC3-associated phagocytosis (LAP)). LAP uses a subset of the autophagy machinery distinct from canonical autophagy. As a result, dying cells are rapidly ingested and degraded and do not induce an autoimmune response. If components of the LAP pathway are lacking, dying cells are not degraded and, hence, the nuclear material escapes, which leads to autoimmune responses. Consequently, a lupus-like systemic inflammatory disease develops.