Type I interferons as regulators of lung inflammation
File(s)
Published version
Author(s)
Makris, S
Paulsen, M
Johansson, C
Type
Journal Article
Abstract
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.
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.
Date Issued
2017-03-10
Date Acceptance
2017-02-21
Citation
Frontiers in Immunology, 2017, 8
ISSN
1664-3224
Publisher
Frontiers Media
Journal / Book Title
Frontiers in Immunology
Volume
8
Copyright Statement
© 2017 Makris, Paulsen and Johansson. This is an open-access article
distributed under the terms of the Creative Commons Attribution License (CC
BY). The use, distribution or reproduction in other forums is permitted, provided
the original author(s) or licensor are credited and that the original publication
in this journal is cited, in accordance with accepted academic practice. No use,
distribution or reproduction is permitted which does not comply with these
terms.
distributed under the terms of the Creative Commons Attribution License (CC
BY). The use, distribution or reproduction in other forums is permitted, provided
the original author(s) or licensor are credited and that the original publication
in this journal is cited, in accordance with accepted academic practice. No use,
distribution or reproduction is permitted which does not comply with these
terms.
Sponsor
Medical Research Council (MRC)
Rosetrees Trust
National Heart and Lung Institute Foundation
National Heart and Lung Institute Foundation
Grant Number
G0800311
M370
Michelle Goritzka
Spiros Makris
Subjects
Science & Technology
Life Sciences & Biomedicine
Immunology
lung
infection
inflammation
type I interferons
pattern recognition receptors
RESPIRATORY SYNCYTIAL VIRUS
TOLL-LIKE RECEPTORS
PATTERN-RECOGNITION RECEPTORS
PLASMACYTOID DENDRITIC CELLS
INNATE IMMUNE GENES
CD8(+) T-CELLS
CYCLIC GMP-AMP
FACTOR-KAPPA-B
RIG-I
CYTOSOLIC DNA
Publication Status
Published
Article Number
259