Skip to main content
. Author manuscript; available in PMC: 2014 Oct 1.
Published in final edited form as: Semin Cancer Biol. 2013 May 30;23(5):329–336. doi: 10.1016/j.semcancer.2013.05.004

Figure. Predicted consequences of LC3 lipidation to different cell-containing vacuoles.

Figure

(A) The lipidation of LC3 (green) to phagosomes (referred to as ‘LAP’) facilitates lysosome fusion (red). For phagosomes harboring dead or dying cells, LC3 lipidation allows for efficient corpses degradation, and is required for an anti-inflammatory response mediated by secreted cytokines. For immunogenic forms of cell death, LC3 lipidation may also facilitate antigen presentation. (B) Vacuoles harboring viable cells engulfed by the cell cannibalism mechanism entosis also exhibit LC3 lipidation that facilitates lysosome fusion and the death of engulfed cells. FcγR-mediated phagocytosis of live tumor cells could also induce LC3 lipidation, which could facilitate tumor cell killing, modulate cytokine secretion or influence antigen presentation. A viable engulfed tumor cell with antibodies bound to its surface is depicted.