Autophagy and inflammatory cell death, partners of innate immunity.
By law in the evolutionary jungle, any host defense mechanism that efficiently kills microbes also exerts a strong selective pressure for tolerant variants to emerge. As a consequence, pathogens can be exploited as powerful tools to examine host defense mechanisms. Recent studies of the confrontation between macrophages and the opportunistic pathogen Legionella pneumophila have revealed a regulatory mechanism that may link autophagy to pyroptosis, a type of programmed cell death. Building from the extensive literature on autophagy, cell death, and innate immunity, we propose here a testable model in which the NOD-LRR protein Naip5 dictates whether murine macrophages elevate autophagy or pyroptosis as a barrier to infection.
Swanson
Michele S
MS
Department of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, USA. mswanson@umich.edu
Molofsky
Ari B
AB
D000818:Animals; D001343:Autophagy; D016923:Cell Death; D007113:Immunity, Innate; D007249:Inflammation / Q000276:immunology / Q000473:pathology*; D016952:Legionella pneumophila / Q000502:physiology; D008264:Macrophages / Q000378:metabolism / Q000382:microbiology*; D051379:Mice; D008954:Models, Biological; D051616:Neuronal Apoptosis-Inhibitory Protein / Q000502:physiology*
C496806:Naip5 protein, mouse; D051616:Neuronal Apoptosis-Inhibitory Protein