title: Interferons and inflammasomes: Cooperation and counterregulation in disease.
abstract: Interferons and the IL-1 family of cytokines have important roles in host defense against invading viruses and bacteria. Inflammasomes, multimeric cytosolic sensors of infection, are required for IL-1β and IL-18 processing and release. Interferons, IL-1β, and IL-18 are also implicated in autoimmune disease and chronic inflammation. Although independent but complementary pathways induce these cytokine subsets during infection, in some circumstances the cross-talk between these key inflammatory mediators is a particular requirement for effective host defense. In this review we will summarize recent discoveries concerning the potentiation of inflammasome responses by type I interferons, particularly in patients with gram-negative bacterial infections, and reflect on the molecular mechanisms of IFN-β's immunosuppressive effects through modulation of inflammasome and IL-1β signaling in patients with tuberculosis and multiple sclerosis.
authors.affiliation: Institute of Innate Immunity, University Hospital, University of Bonn, Bonn, Germany.
authors.forename: Larisa I
authors.initials: LI
authors.lastname: Labzin
authors.affiliation: Institute of Innate Immunity, University Hospital, University of Bonn, Bonn, Germany.
authors.forename: Mario A R
authors.initials: MA
authors.lastname: Lauterbach
authors.affiliation: Institute of Innate Immunity, University Hospital, University of Bonn, Bonn, Germany; Department of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Mass; German Center for Neurodegenerative Diseases, Bonn, Germany; Centre of Molecular Inflammation Research, Norwegian University of Science and Technology, Trondheim, Norway. Electronic address: eicke.latz@uni-bonn.de.
authors.forename: Eicke
authors.initials: E
authors.lastname: Latz
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000209:etiology / Q000378:metabolism; D020169:Caspases / Q000378:metabolism; D054884:Host-Pathogen Interactions / Q000276:immunology; D006801:Humans; D058847:Inflammasomes / Q000378:metabolism*; D007249:Inflammation / Q000209:etiology / Q000378:metabolism; D007372:Interferons / Q000378:metabolism*; D020382:Interleukin-18 / Q000378:metabolism; D053583:Interleukin-1beta / Q000378:metabolism; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein / Q000378:metabolism; D015398:Signal Transduction
chemical_list: D058847:Inflammasomes; D020382:Interleukin-18; D053583:Interleukin-1beta; D000071199:NLR Family, Pyrin Domain-Containing 3 Protein; D007372:Interferons; D020169:Caspases
keywords: AIM2; IL-18; IL-1β; Interferon; NLRP3; caspase-1; caspase-11; experimental autoimmune encephalomyelitis; gram-negative bacteria; guanylate-binding protein; inflammasome; multiple sclerosis; pyroptosis; tuberculosis