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Type I interferons in infectious disease
Open accessAbstract
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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“If type I IFNs are present early and properly localized to sites of infection, they can effectively limit viral propagation, as type I IFNs are responsible for optimal activation of macrophages, antigen presentation by DCs, and enhanced anti-viral effector T cell responses106.”
From SARS-CoV-2, COVID-19 and the aging immune system (2021) · cites this paper as [106]
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Metadata
- 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)
- Venue
- Nature Reviews Immunology
- Published
- 2015-01-23
- Volume
- 15
- Issue
- 2
- Pages
- 87-103
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- 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
- 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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