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J Allergy Clin Immunol. 2016 Jul;138(1):37-46. doi: 10.1016/j.jaci.2016.05.010. Epub 2016 May 24.

Interferons and inflammasomes: Cooperation and counterregulation in disease.

Author information

1
Institute of Innate Immunity, University Hospital, University of Bonn, Bonn, Germany.
2
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.

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.

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

PMID:
27373324
DOI:
10.1016/j.jaci.2016.05.010
[Indexed for MEDLINE]

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