Type I interferons in infectious disease

By Finlay W Mcnab, K. Mayer-Barber, A. Sher, A. Wack, A. O’Garra. Nature reviews. Immunology, 2015

2,491 citations recorded by the source corpus.

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.

Subfields: Cardiology and Cardiovascular Medicine, Hepatology, Immunology

View Paper: https://www.semanticscholar.org/paper/b447c0faf6d40f112c37a77825d0aed3dccec03c

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In Cardiology and Cardiovascular Medicine

J. Molkentin

In Hepatology

In Immunology

Citations in the corpus

Single cell RNA sequencing of 13 human tissues identify cell types and receptors of human coronaviruses (2020, background): “Generally, virally infected cells release interferons to suppress viral activities [36-38].”
CD8 T Cell Exhaustion During Chronic Viral Infection and Cancer. (2019, background): “IFN-α/β are critical proinflammatory cytokines that can suppress viral replication through direct induction of antiviral activities and by activating innate immune cells (177).”
The senescence-associated secretory phenotype and its physiological and pathological implications (2024, neutral): “Cellular senescence involves de-repression of LINE1 elements, which activate a type I interferon response that acts on innate immunity cells 177 .”
Dysregulated type I interferon and inflammatory monocyte-macrophage responses cause lethal pneumonia in SARS-CoV-infected mice (2016, background): “…viral infections, it has become increasingly evident that IFN-I also promotes detrimental inflammatory responses in some bacterial, fungal, and chronic virus infections through a complex array of mechanisms that tend to be pathogen specific (Carrero, 2013; McNab et al., 2015; Trinchieri, 2010).”
Autophagy in inflammation, infection, and immunometabolism (2021, background): “Most cells in the body can produce type I IFN using various systems, of which cGAS-STING and TLR-TRIF, RIG-I-MAVS targeted by autophagy as discussed above, are some of the key pathways (McNab et al., 2015).”
Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “Further underscoring the complexity of the interaction between inflammation and pyroptosis [649], CASP11 can also be upregulated by a complement cascade dependent on carboxypeptidase B1 (CPB1) acting downstream of TLR4 and IFNAR1 activation [650].”