The β2 Integrin Mac-1 Induces Protective LC3-Associated Phagocytosis of Listeria monocytogenes

What is it about?

The intracellular pathogen Listeria monocytogenes (L.m.) is targeted by the autophagic machinery, but the molecular mechanisms involved and consequences for anti-listerial immunity remain enigmatic. Here, we demonstrate that L.m. infection of macrophages in vivo exclusively evokes LC3-associated phagocytosis (LAP), but not canonical autophagy, and that targeting of L.m. by LAP is required for anti-listerial immunity. The pathway leading to LAP induction in response to L.m. infection

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Why is it important?

L.m. are exclusively targeted by LAP, which contributes to anti-listerial immunity. Mechanistically, by using a respective panel of knockout mice, we delineate a pathway for induction of LAP: Interaction of L.m. with the β2 integrin Mac-1 induces activation of ASMase, which is essentially required for Nox2 activation and subsequent LC3 recruitment to L.m.-containing phagosomes. LAP then promotes fusion of L.m.-containing phagosomes with lysosomes, which increases exposure of L.m. to bactericidal lysosomal acid hydrolases, thereby enhancing anti-listerial immunity in mice.