title: The inflammasome NLRs in immunity, inflammation, and associated diseases.
abstract: Inflammasome activation leads to caspase-1 activation, which causes the maturation and secretion of pro-IL-1β and pro-IL-18 among other substrates. A subgroup of the NLR (nucleotide-binding domain, leucine-rich repeat containing) proteins are key mediators of the inflammasome. Studies of gene-deficient mice and cells have implicated NLR inflammasomes in a host of responses to a wide range of microbial pathogens, inflammatory diseases, cancer, and metabolic and autoimmune disorders. Determining exactly how the inflammasome is activated in these diseases and disease models remains a challenge. This review presents and integrates recent progress in the field.
authors.affiliation: Department of Microbiology and Immunology, Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, 27599, USA. antigen@med.unc.edu
authors.forename: Beckley K
authors.initials: BK
authors.lastname: Davis
authors.forename: Haitao
authors.initials: H
authors.lastname: Wen
authors.forename: Jenny P-Y
authors.initials: JP
authors.lastname: Ting
mesh_terms: D000818:Animals; D006801:Humans; D058847:Inflammasomes / Q000276:immunology*; D007249:Inflammation / Q000276:immunology*; D018836:Inflammation Mediators / Q000276:immunology; D036341:Intercellular Signaling Peptides and Proteins / Q000276:immunology*; D008659:Metabolic Diseases / Q000276:immunology; D009369:Neoplasms / Q000276:immunology
chemical_list: D058847:Inflammasomes; D018836:Inflammation Mediators; D036341:Intercellular Signaling Peptides and Proteins