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. 2021 Apr 14;53(4):528–536. doi: 10.1038/s12276-021-00600-3

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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 — A Recognition of extracellular pathogens activates the PI3KC3-UVRAG-Rubicon complex to generate PI3P on the engulfing phagosome. Rubicon-mediated PI3P generation stabilizes and activates the Rubicon-interacting NOX2 complex, thereby generating ROS. PI3P and ROS activate the Atg5-Atg12 conjugation system, thereby embedding LC3-PE in the phagosome membrane. LC3-embedded phagosomes (LAPosomes) fuse with lysosomes to degrade the engulfed pathogens. B Rubicon interacts with CARD9, thereby repressing the M-CMB complex, which is important for the generation of proinflammatory signals.