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Type I interferons as regulators of lung inflammation

Immune responses to lung infections must be tightly regulated in order to permit pathogen eradication while maintaining organ function. Exuberant or dysregulated inflammation can impair gas exchange and underlies many instances of lung disease. An important driver of inflammation in the lung is the...

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Hauptverfasser: Makris, Spyridon (VerfasserIn) , Paulsen, Michelle (VerfasserIn) , Johansson, Cecilia (VerfasserIn)
Dokumenttyp: Article (Journal)
Sprache:Englisch
Veröffentlicht: 10 March 2017
In: Frontiers in immunology
Year: 2017, Jahrgang: 8
ISSN:1664-3224
DOI:10.3389/fimmu.2017.00259
Online-Zugang:Verlag, Volltext: http://dx.doi.org/10.3389/fimmu.2017.00259
Verlag, Volltext: https://www.frontiersin.org/articles/10.3389/fimmu.2017.00259/full
Volltext
Verfasserangaben:Spyridon Makris, Michelle Paulsen and Cecilia Johansson

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520 |a Immune responses to lung infections must be tightly regulated in order to permit pathogen eradication while maintaining organ function. Exuberant or dysregulated inflammation can impair gas exchange and underlies many instances of lung disease. An important driver of inflammation in the lung is the interferon (IFN) response. Type I IFNs are anti-viral cytokines that induce a large range of proteins that impair viral replication in infected cells. This cell-intrinsic action plays a crucial role in protecting the lungs from spread of respiratory viruses. However, type I IFNs have also recently been found to be central to the initiation of lung inflammatory responses, by inducing recruitment and activation of immune cells. This helps control virus burden but can cause detrimental immunopathology and contribute to disease severity. Furthermore, there is now increasing evidence that type I IFNs are not only induced after viral infections but also after infection with bacteria and fungi. The pro-inflammatory function of type I IFNs in the lung opens up the possibility of immune modulation directed against this anti-viral cytokine family. In this review, the initiation and signaling of type I IFNs as well as their role in driving and maintaining lung inflammation will be discussed. 
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