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IL-18 associated wi...
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Briend, EmmanuelAgenus Ltd,MedImmune Limited, Cambridge
(författare)
IL-18 associated with lung lymphoid aggregates drives IFNγ production in severe COPD
- Artikel/kapitelEngelska2017
Förlag, utgivningsår, omfång ...
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2017-08-22
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Springer Science and Business Media LLC,2017
Nummerbeteckningar
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LIBRIS-ID:oai:lup.lub.lu.se:d1b8d881-9e90-40eb-80ef-81e1c48e53dd
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https://lup.lub.lu.se/record/d1b8d881-9e90-40eb-80ef-81e1c48e53ddURI
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https://doi.org/10.1186/s12931-017-0641-7DOI
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Språk:engelska
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Sammanfattning på:engelska
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Ämneskategori:art swepub-publicationtype
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Ämneskategori:ref swepub-contenttype
Anmärkningar
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Background: Increased interferon gamma (IFNγ) release occurs in Chronic Obstructive Pulmonary Disease (COPD) lungs. IFNγ supports optimal viral clearance, but if dysregulated could increase lung tissue destruction. Methods: The present study investigates which mediators most closely correlate with IFNγ in sputum in stable and exacerbating disease, and seeks to shed light on the spatial requirements for innate production of IFNγ, as reported in mouse lymph nodes, to observe whether such microenvironmental cellular organisation is relevant to IFNγ production in COPD lung. Results: We show tertiary follicle formation in severe disease alters the dominant mechanistic drivers of IFNγ production, because cells producing interleukin-18, a key regulator of IFNγ, are highly associated with such structures. Interleukin-1 family cytokines correlated with IFNγ in COPD sputum. We observed that the primary source of IL-18 in COPD lungs was myeloid cells within lymphoid aggregates and IL-18 was increased in severe disease. IL-18 released from infected epithelium or from activated myeloid cells, was more dominant in driving IFNγ when IL-18-producing and responder cells were in close proximity. Conclusions: Unlike tight regulation to control infection spread in lymphoid organs, this local interface between IL-18-expressing and responder cell is increasingly supported in lung as disease progresses, increasing its potential to increase tissue damage via IFNγ.
Ämnesord och genrebeteckningar
Biuppslag (personer, institutioner, konferenser, titlar ...)
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Ferguson, G. JohnMedImmune Limited, Cambridge
(författare)
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Mori, MichikoLund University,Lunds universitet,Luftvägsinflammation,Forskargrupper vid Lunds universitet,Airway Inflammation and Immunology,Lund University Research Groups(Swepub:lu)med-mhm
(författare)
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Damera, GautamMedImmune, Inc.
(författare)
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Stephenson, KatherineUniversity of Nottingham,MedImmune Limited, Cambridge
(författare)
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Karp, Natasha A.AstraZeneca, UK
(författare)
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Sethi, SanjayThe State University of New York
(författare)
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Ward, Christine KMedImmune, Inc.,Bristol-Myers Squibb
(författare)
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Sleeman, Matthew A.MedImmune Limited, Cambridge,Regeneron Pharmaceuticals, Inc.
(författare)
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Erjefält, Jonas S.Lund University,Lunds universitet,Luftvägsinflammation,Forskargrupper vid Lunds universitet,Airway Inflammation and Immunology,Lund University Research Groups,Skåne University Hospital(Swepub:lu)mphy-jer
(författare)
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Finch, Donna K.MedImmune Limited, Cambridge
(författare)
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Agenus LtdMedImmune Limited, Cambridge
(creator_code:org_t)
Sammanhörande titlar
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Ingår i:Respiratory Research: Springer Science and Business Media LLC18:11465-99211465-993X
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Briend, Emmanuel
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Ferguson, G. Joh ...
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Mori, Michiko
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Damera, Gautam
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Stephenson, Kath ...
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Karp, Natasha A.
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visa fler...
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Sethi, Sanjay
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Ward, Christine ...
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Sleeman, Matthew ...
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Erjefält, Jonas ...
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Finch, Donna K.
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- MEDICIN OCH HÄLSOVETENSKAP
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och Klinisk medicin
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Respiratory Rese ...
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Lunds universitet