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Interleukin-6 limits influenza-induced inflammation and protects against fatal lung pathology

By Sarah Nicol Lauder, Emma Jones, Kathryn Smart, Anja Constanze Bloom, Anwen Sian Williams, James P. Hindley, Beatrice Ondondo, Philip Russel Taylor, Mathew Clement, Ceri Alan Fielding, Andrew James Godkin, Simon Arnett Jones and Awen Myfanwy Gallimore

Abstract

Balancing the generation of immune responses capable of controlling virus replication with those causing immunopathology is critical for the survival of the host and resolution of influenza-induced inflammation. Based on the capacity of interleukin-6 (IL-6) to govern both optimal T-cell responses and inflammatory resolution, we hypothesised that IL-6 plays an important role in maintaining this balance. Comparison of innate and adaptive immune responses in influenza-infected wild-type control and IL-6-deficient mice revealed striking differences in virus clearance, lung immunopathology and generation of heterosubtypic immunity. Mice lacking IL-6 displayed a profound defect in their ability to mount an anti-viral T-cell response. Failure to adequately control virus was further associated with an enhanced infiltration of inflammatory monocytes into the lung and an elevated production of the pro-inflammatory cytokines, IFN-α and TNF-α. These events were associated with severe lung damage, characterised by profound vascular leakage and death. Our data highlight an essential role for IL-6 in orchestrating anti-viral immunity through an ability to limit inflammation, promote protective adaptive immune responses and prevent fatal immunopathology

Topics: QR180 Immunology, RM Therapeutics. Pharmacology
Publisher: 'Wiley'
Year: 2013
DOI identifier: 10.1002/eji.201243018
OAI identifier: oai:http://orca.cf.ac.uk:58531
Provided by: ORCA
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