title: Molecular mechanisms regulating NLRP3 inflammasome activation.
abstract: Inflammasomes are multi-protein signaling complexes that trigger the activation of inflammatory caspases and the maturation of interleukin-1β. Among various inflammasome complexes, the NLRP3 inflammasome is best characterized and has been linked with various human autoinflammatory and autoimmune diseases. Thus, the NLRP3 inflammasome may be a promising target for anti-inflammatory therapies. In this review, we summarize the current understanding of the mechanisms by which the NLRP3 inflammasome is activated in the cytosol. We also describe the binding partners of NLRP3 inflammasome complexes activating or inhibiting the inflammasome assembly. Our knowledge of the mechanisms regulating NLRP3 inflammasome signaling and how these influence inflammatory responses offers further insight into potential therapeutic strategies to treat inflammatory diseases associated with dysregulation of the NLRP3 inflammasome.
authors.affiliation: Department of Microbiology, Chungnam National University School of Medicine, Daejeon 301-747, South Korea.|Infection Signaling Network Research Center, Chungnam National University School of Medicine, Daejeon 301-747, South Korea.
authors.forename: Eun-Kyeong
authors.initials: EK
authors.lastname: Jo
authors.affiliation: Department of Microbiology, Chungnam National University School of Medicine, Daejeon 301-747, South Korea.|Infection Signaling Network Research Center, Chungnam National University School of Medicine, Daejeon 301-747, South Korea.
authors.forename: Jin Kyung
authors.initials: JK
authors.lastname: Kim
authors.affiliation: Department of Microbiology, Chungnam National University School of Medicine, Daejeon 301-747, South Korea.|Infection Signaling Network Research Center, Chungnam National University School of Medicine, Daejeon 301-747, South Korea.
authors.forename: Dong-Min
authors.initials: DM
authors.lastname: Shin
authors.affiliation: Medical Mycology Research Center, Chiba University, Chiba 260-8673, Japan.|Nippon Institute for Biological Science, Tokyo 198-0024, Japan.
authors.forename: Chihiro
authors.initials: C
authors.lastname: Sasakawa
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology* / Q000473:pathology; D003600:Cytosol / Q000276:immunology* / Q000473:pathology; D006801:Humans; D058847:Inflammasomes / Q000276:immunology*; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D053583:Interleukin-1beta / Q000276:immunology; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein / Q000276:immunology* / Q000378:metabolism; D015398:Signal Transduction / Q000276:immunology*
chemical_list: C508585:IL1B protein, human; D058847:Inflammasomes; D053583:Interleukin-1beta; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; C453881:NLRP3 protein, human