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Nat Rev Immunol. 2014 Jan;14(1):36-49. doi: 10.1038/nri3581.

Regulation of type I interferon responses.

Author information

1
1] Arthritis and Tissue Degeneration Program and the David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York 10021, USA. [2] Immunology and Microbial Pathogenesis Program, Weill Cornell Graduate School of Medical Sciences, New York, New York 10065, USA. [3] Department of Medicine, Weill Cornell Medical College, New York, New York 10065,USA.
2
Arthritis and Tissue Degeneration Program and the David Z. Rosensweig Genomics Research Center, Hospital for Special Surgery, New York, New York 10021, USA.

Abstract

Type I interferons (IFNs) activate intracellular antimicrobial programmes and influence the development of innate and adaptive immune responses. Canonical type I IFN signalling activates the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway, leading to transcription of IFN-stimulated genes (ISGs). Host, pathogen and environmental factors regulate the responses of cells to this signalling pathway and thus calibrate host defences while limiting tissue damage and preventing autoimmunity. Here, we summarize the signalling and epigenetic mechanisms that regulate type I IFN-induced STAT activation and ISG transcription and translation. These regulatory mechanisms determine the biological outcomes of type I IFN responses and whether pathogens are cleared effectively or chronic infection or autoimmune disease ensues.

PMID:
24362405
PMCID:
PMC4084561
DOI:
10.1038/nri3581
[Indexed for MEDLINE]
Free PMC Article

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