LC3-associated phagocytosis initiated by integrin ITGAM-ITGB2/Mac-1 enhances immunity to Listeria monocytogenes. Issue 8 (3rd August 2018)

• Record Type: Journal Article
• Authors: Herb, Marc; Gluschko, Alexander; Schramm, Michael
• Is Part Of: Autophagy. Volume 14:Issue 8(2018)
• Page Start: 1462
• Page End: 1464
• Publication Date: 2018-08-03
• Subjects: ß2 integrin Mac-1/CR3 -- acid sphingomyelinase -- LC3-associated phagocytosis -- Listeria monocytogenes -- lysosome -- macrophages -- NAPDH oxidase Nox2 -- noncanonical autophagy -- reactive oxygen species; Autophagic vacuoles -- Periodicals; Apoptosis -- Periodicals; Cell death -- Periodicals; Lysosomes -- Periodicals; Degeneration (Pathology) -- Periodicals; Autophagy -- Periodicals; Cell Death -- Periodicals; Lysosomes -- Periodicals; Periodicals; 571.936
• DOI: 10.1080/15548627.2018.1475816
• Languages: English
• ISSNs: 1554-8627

Abstract

ABSTRACT: The macroautophagic/autophagic machinery cannot only target cell-endogenous components but also intracellular pathogenic bacteria such as Listeria monocytogenes. Listeria are targeted both by canonical autophagy and by a noncanonical form of autophagy referred to as LC3-associated phagocytosis (LAP). The molecular mechanisms involved and whether these processes contribute to anti-listerial immunity or rather provide Listeria with a replicative niche for persistent infection, however, remained unknown. Recently, using an in vivo mouse infection model, we have been able to demonstrate that Listeria in tissue macrophages are targeted exclusively by LAP. Furthermore, our data show that LAP is required for killing of Listeria by macrophages and thereby contributes to anti-listerial immunity of mice, whereas canonical autophagy is completely dispensable. Moreover, we have elucidated the molecular mechanisms that trigger LAP of Listeria and identified the integrin ITGAM-ITGB2/Mac-1/CR3/integrin αM ß2 as the receptor that initiates LAP in response to Listeria infection.