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Interferons: Signaling, antiviral and viral evasion
Open accessAbstract
Interferons (IFNs) were discovered as antiviral agents 50 years ago, and enormous progress has been made since then. Nowadays, IFNs (specifically type I IFNs), have been ascribed as the cytokines that bridge the innate and adaptive immunity soon after the recognition of pathogen-associated molecular patterns (PAMPs) by the infected host. Notably, a unifying mechanism for type I IFN production has been established upon innate immune detection. Thus, TLR 3, 4, 7 and 9 associate endosomal recognition of PAMPs to type I IFN responses, a mechanism that has been shown in plasmacytoid dendritic cells to be dependent on the PI3K/mTOR/S6K pathway. It is worth noting that pathogen recognition triggers a fine-tuned controlled program that not only includes the production of antiviral (IFN) and pro-inflammatory cytokines to initiate the antiviral response but also signals the cessation of the response through the induction of suppressors of cytokine signaling (SOCS). SOCS in turn is under tight regulation of the TAM receptors (protein tyrosine kinase receptors TYRO3, AXL and MER), and activation of which thereby protects the host from the threats of autoimmune diseases.
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“This is critical from the host perspective, as the virus-induced secretion of signaling factors mediates the onset of innate and adaptive immunity (116).”
From The Impact of Mass Spectrometry–Based Proteomics on Fundamental Discoveries in Virology (2014) · cites this paper as [116]
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Metadata
- Authors
- Bonjardim, C. A., Ferreira, P. C. P., & Kroon, E. G.
- Affiliations
- Universidade Federal de Minas Gerais (BR)
- Corresponding author
- Bonjardim, Cláudio A.
- Venue
- Immunology Letters
- Publisher
- Elsevier BV
- Published
- 2009-01
- Volume
- 122
- Issue
- 1
- Pages
- 1-11
- ISSN
- 0165-2478 (ISSN-L)
- PMC
- PMC7112942
- OpenAlex
- W2020464368
- Cited by
- 196
- References
- 163
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 7 · 2023: 5 · 2022: 11 · 2021: 5 · 2020: 6 · 2019: 10 · 2018: 2 · 2017: 11 · 2016: 11 · 2015: 15 · 2014: 16 · 2013: 19 · 2012: 23
- FWCI
- 1.10
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Immunology Letters (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- 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
- interferon, type I interferon, antiviral signaling, viral evasion, innate immunity, adaptive immunity, pathogen-associated molecular patterns, Toll-like receptors, plasmacytoid dendritic cells, suppressor of cytokine signaling, TAM receptors, autoimmune disease
- MeSH terms
- Animals, Humans, Immunity, Innate, Interferon Type I, Endosomes, Virus Diseases, Signal Transduction, Feedback, Physiological, Suppressor of Cytokine Signaling Proteins, Toll-Like Receptors, Host-Pathogen Interactions
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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