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LAP it up, fuzz ball: a short history of LC3-associated phagocytosis
1Immunity, Inflammation, and Disease Laboratory, National Institute of Environmental Health Sciences, 111 T.W. Alexander Drive, Research Triangle Park, NC, USA.
Abstract:
LC3-associated phagocytosis (LAP) exists at the crossroads of the two evolutionary pathways of phagocytosis and autophagy. When a phagocyte engulfs an extracellular particle that engages receptor signaling, components of the autophagy machinery and Rubicon are recruited to the cargo-containing phagosome or LAPosome. Formation of the LAPosome is critical for both cargo clearance as well as mediating the proper signaling cascade. Globally, LAP functions as an immunosuppressive mechanism, as LAP deficiency often results in hyperinflammation. As defects in the autophagy machinery have been long associated with aberrant immune responses and autoimmune disorders, it is vital that we now revisit these associations with forms of non-canonical autophagy, like LAP, in mind.
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