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How location and cellular signaling combine to activate the NLRP3 inflammasome
Authors:Anil Akbal,Alesja Dernst,Marta Lovotti,Matthew S. J. Mangan,Ró  isí  n M. McManus,Eicke Latz
Affiliation:1.Institute of Innate Immunity, University Hospital Bonn, University of Bonn, 53127 Bonn, Germany ;2.German Center for Neurodegenerative Diseases, 53127 Bonn, Germany ;3.Department of Infectious Diseases & Immunology, UMass Medical School, Worcester, MA 01605 USA ;4.Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, 7491 Trondheim, Norway
Abstract:NOD-, LRR-, and pyrin domain-containing 3 (NLRP3) is a cytosolic innate immune sensor of cellular stress signals, triggered by infection and sterile inflammation. Upon detection of an activating stimulus, NLRP3 transitions from an inactive homo-oligomeric multimer into an active multimeric inflammasome, which promotes the helical oligomeric assembly of the adaptor molecule ASC. ASC oligomers provide a platform for caspase-1 activation, leading to the proteolytic cleavage and activation of proinflammatory cytokines in the IL-1 family and gasdermin D, which can induce a lytic form of cell death. Recent studies investigating both the cellular requirement for NLRP3 activation and the structure of NLRP3 have revealed the complex regulation of NLRP3 and the multiple steps involved in its activation. This review presents a perspective on the biochemical and cellular processes controlling the assembly of the NLRP3 inflammasome with particular emphasis on structural regulation and the role of organelles. We also highlight the latest research on metabolic control of this inflammatory pathway and discuss promising clinical targets for intervention.
Keywords:NLRP3   Inflammasome   Mechanism   Localization   Structure   Regulation
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