title: Inflammasomes and autoimmunity.
abstract: The NOD-like receptor (NLR) family members are cytosolic sensors of microbial components and danger signals. A subset of NLRs control inflammasome assembly that results in caspase-1 activation and, in turn, IL-1β and IL-18 production. Excessive inflammasome activation can cause autoinflammatory disorders, including the hereditary periodic fevers. Autoinflammatory and autoimmune diseases form a disease spectrum of aberrant, immune-mediated inflammation against self, through innate and adaptive immunity. However, the role of inflammasomes in autoimmune disease is less clear than in autoinflammation, despite the numerous effects IL-1β and IL-18 can have on shaping adaptive immunity. We summarize the role of inflammasomes in autoimmune disorders, highlight the need for a better understanding of inflammasomes in these conditions and offer suggestions for future research directions.
authors.affiliation: Department of Immunology, St. Jude Children's Research Hospital, MS #351, Suite E7004, 262 Danny Thomas Place, Memphis, TN 38105, USA.
authors.forename: Patrick J
authors.initials: PJ
authors.lastname: Shaw
authors.forename: Michael F
authors.initials: MF
authors.lastname: McDermott
authors.forename: Thirumala-Devi
authors.initials: TD
authors.lastname: Kanneganti
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology; D015551:Autoimmunity / Q000235:genetics / Q000276:immunology*; D006801:Humans; D058847:Inflammasomes / Q000276:immunology*
chemical_list: D058847:Inflammasomes