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Nat Rev Immunol. 2015 Feb;15(2):87-103. doi: 10.1038/nri3787.

Type I interferons in infectious disease.

Author information

1
1] Allergic Inflammation Discovery Performance Unit, Respiratory Disease Respiratory Research and Development, GlaxoSmithKline, Stevenage, Hertfordshire SG1 2NY, UK. [2] Division of Immunoregulation, Medical Research Council (MRC) National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
2
Immunobiology Section, Laboratory of Parasitic Diseases (LPD), National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH), Bethesda, Maryland 20892, USA.
3
Division of Immunoregulation, Medical Research Council (MRC) National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.
4
1] Division of Immunoregulation, Medical Research Council (MRC) National Institute for Medical Research, Mill Hill, London NW7 1AA, UK. [2] National Heart and Lung Institute (NHLI), Faculty of Medicine, Imperial College London, London, UK.

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 IFN╬│, 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.

PMID:
25614319
DOI:
10.1038/nri3787
[Indexed for MEDLINE]

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