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. Author manuscript; available in PMC: 2019 Feb 1.
Published in final edited form as: Curr Opin Immunol. 2017 Nov 7;50:21–31. doi: 10.1016/j.coi.2017.10.004

Figure 2. Xenophagy versus LC3-associated phagocytosis.

Figure 2

(Left) During xenophagy, rupture of the pathogen-containing vesicle triggers the recruitment of ubiquitin to endosomal proteins or the pathogen itself. subsequently, autophagy adaptors, like p62, OPTN, and NDP52, are recruited and link these ubiquitinated pathogen substrates to the LC3-containing autophagosome. In addition, ATG proteins and other autophagy components are recruited via ubiquitin to mediate autophagosome formation. (Right) During LC3-associated phagocytosis (LAP), engagement of the PRRs during uptake of a pathogen triggers the recruitment of the Class III PI3K complex, comprised of VSP34, Beclin 1, UVRAG, and Rubicon, to the single membraned LAPosome. This complex is required for sustained and localized production of PI3P, which is needed for the recruitment of the downstream LAP machinery (like ATG5, ATG12, ATG16L, and ATG7) and stabilization of the NOX2 complex for ROS production. Both ROS and PI3P are required for successful LC3-PE decoration of the LAPosome. In both scenarios, LC3-PE is required for fusion to the lysosome and subsequent degradation of its contents.