Cited by 2,780interferon and immune responsesImmune Response and InflammationCytokine Signaling Pathways and Interactions

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Type I interferons in infectious disease

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McNab, Finlay, Mayer-Barber, Katrin, Sher, Alan, Wack, Andreas, O'Garra, Anne·2015·Nature Reviews Immunology

DOI 10.1038/nri3787PMC PMC7162685

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Abstract

Type I interferons (IFNs) have diverse effects on innate and adaptive immune cells during infection with viruses, bacteria, parasites and fungi, directly and/or indirectly through the induction of other mediators. Type I IFNs are important for host defence against viruses. However, recently, they have been shown to cause immunopathology in some acute viral infections, such as influenza virus infection. Conversely, they can lead to immunosuppression during chronic viral infections, such as lymphocytic choriomeningitis virus infection. During bacterial infections, low levels of type I IFNs may be required at an early stage, to initiate cell-mediated immune responses. High concentrations of type I IFNs may block B cell responses or lead to the production of immunosuppressive molecules, and such concentrations also reduce the responsiveness of macrophages to activation by IFNγ, as has been shown for infections with Listeria monocytogenes and Mycobacterium tuberculosis. Recent studies in experimental models of tuberculosis have demonstrated that prostaglandin E2 and interleukin-1 inhibit type I IFN expression and its downstream effects, demonstrating that a cross-regulatory network of cytokines operates during infectious diseases to provide protection with minimum damage to the host.

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Authors: McNab, F., Mayer-Barber, K., Sher, A., Wack, A., & O'Garra, A.
Affiliations: GlaxoSmithKline (United Kingdom) (GB)
National Institutes of Health (US)
National Institute for Medical Research (GB)
ORCID: Mayer-Barber, Katrin
Sher, Alan
Wack, Andreas
Venue: Nature Reviews Immunology
Publisher: Springer Science and Business Media LLC
Published: 2015-01-23
Volume: 15
Issue: 2
Pages: 87-103
ISSN: 1474-1733 (ISSN-L)
1474-1741
DOI: 10.1038/nri3787
PMC: PMC7162685
OpenAlex: W2091129202
Cited by: 2,780
References: 238
Citations by year: 2026: 263 · 2025: 333 · 2024: 364 · 2023: 330 · 2022: 330 · 2021: 307 · 2020: 194 · 2019: 160 · 2018: 166 · 2017: 169 · 2016: 119 · 2015: 44
FWCI: 15.67
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: www.springernature.com/gp/researchers/text-and-data-mining (tdm)
www.springernature.com/gp/researchers/text-and-data-mining (vor)
Locations: Nature reviews. Immunology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: Wellcome Trust (FC001126)
Francis Crick Institute (10206, 10126)
Cancer Research UK (FC001126)
National Institutes of Health
Medical Research Council (U117597139, U117565642)
National Institute of Allergy and Infectious Diseases
FP7 Ideas: European Research Council (294682)
Topics: Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
Keywords: type I interferon, innate immunity, viral infection, bacterial infection, parasitic infection, fungal infection, immunopathology, influenza virus, lymphocytic choriomeningitis virus, chronic viral infection, immunosuppression, B cell response, macrophage activation, Listeria monocytogenes, Mycobacterium tuberculosis, prostaglandin E2, interleukin-1, host defense
MeSH terms: Animals, Bacterial Infections, Communicable Diseases, Humans, Interferon Type I, Mycoses, Parasitic Diseases, Virus Diseases, Signal Transduction

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