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Eur J Immunol. 2013 Jul 15. doi: 10.1002/eji.201243018. [Epub ahead of print]
Interleukin-6 limits influenza-induced inflammation and protects against fatal lung pathology.
Lauder SN, Jones E, Smart K, Bloom A, Williams AS, Hindley JP, Ondondo B, Taylor PR, Clement M, Fielding C, Godkin AJ, Jones SA, Gallimore AM.
Source
Cardiff Institute of Infection and Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff, UK.
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. This article is protected by copyright. All rights reserved This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
Adaptive Immunity, Heterosubtypic Immunity, IL-6, Innate Immunity, Pulmonary Damage
PMID:
23857287
[PubMed - as supplied by publisher]
Interleukin-6 limits influenza-induced inflammation and protects against fatal lung pathology.
Lauder SN, Jones E, Smart K, Bloom A, Williams AS, Hindley JP, Ondondo B, Taylor PR, Clement M, Fielding C, Godkin AJ, Jones SA, Gallimore AM.
Source
Cardiff Institute of Infection and Immunity, School of Medicine, Cardiff University, Heath Park, Cardiff, UK.
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. This article is protected by copyright. All rights reserved This article is protected by copyright. All rights reserved.
This article is protected by copyright. All rights reserved.
KEYWORDS:
Adaptive Immunity, Heterosubtypic Immunity, IL-6, Innate Immunity, Pulmonary Damage
PMID:
23857287
[PubMed - as supplied by publisher]
