Journal
NATURE REVIEWS IMMUNOLOGY
Volume 14, Issue 1, Pages 36-49Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nri3581
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Funding
- US National Institutes of Health
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI046712, R01AI044938] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES [K01AR066063, R01AR050401, R01AR046713] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL & CRANIOFACIAL RESEARCH [R01DE019420] Funding Source: NIH RePORTER
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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.
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