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Cigarette smoke sil...
Cigarette smoke silences innate lymphoid cell function and facilitates an exacerbated type I interleukin-33-dependent response to infection.
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Kearley, Jennifer (author)
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Silver, Jonathan S (author)
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- Sandén, Caroline (author)
- Lund University,Lunds universitet,Luftvägsinflammation,Forskargrupper vid Lunds universitet,Airway Inflammation and Immunology,Lund University Research Groups
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Liu, Zheng (author)
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Berlin, Aaron A (author)
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White, Natalie (author)
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- Mori, Michiko (author)
- Lund University,Lunds universitet,Luftvägsinflammation,Forskargrupper vid Lunds universitet,Airway Inflammation and Immunology,Lund University Research Groups
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Pham, Tuyet-Hang (author)
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Ward, Christine K (author)
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Criner, Gerard J (author)
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Marchetti, Nathaniel (author)
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Mustelin, Tomas (author)
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- Erjefält, Jonas (author)
- Lund University,Lunds universitet,Luftvägsinflammation,Forskargrupper vid Lunds universitet,Airway Inflammation and Immunology,Lund University Research Groups
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Kolbeck, Roland (author)
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Humbles, Alison A (author)
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(creator_code:org_t)
- Elsevier BV, 2015
- 2015
- English.
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In: Immunity. - : Elsevier BV. - 1074-7613. ; 42:3, s. 566-579
- Related links:
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http://www.ncbi.nlm....
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http://dx.doi.org/10...
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http://www.cell.com/...
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https://doi.org/10.1...
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Abstract
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- Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease and is presumed to be central to the altered responsiveness to recurrent infection in these patients. We examined the effects of smoke priming underlying the exacerbated response to viral infection in mice. Lack of interleukin-33 (IL-33) signaling conferred complete protection during exacerbation and prevented enhanced inflammation and exaggerated weight loss. Mechanistically, smoke was required to upregulate epithelial-derived IL-33 and simultaneously alter the distribution of the IL-33 receptor ST2. Specifically, smoke decreased ST2 expression on group 2 innate lymphoid cells (ILC2s) while elevating ST2 expression on macrophages and natural killer (NK) cells, thus altering IL-33 responsiveness within the lung. Consequently, upon infection and release, increased local IL-33 significantly amplified type I proinflammatory responses via synergistic modulation of macrophage and NK cell function. Therefore, in COPD, smoke alters the lung microenvironment to facilitate an alternative IL-33-dependent exaggerated proinflammatory response to infection, exacerbating disease.
Subject headings
- MEDICIN OCH HÄLSOVETENSKAP -- Medicinska och farmaceutiska grundvetenskaper -- Immunologi inom det medicinska området (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Basic Medicine -- Immunology in the medical area (hsv//eng)
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- art (subject category)
- ref (subject category)
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Immunity
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- By the author/editor
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Kearley, Jennife ...
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Silver, Jonathan ...
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Sandén, Caroline
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Liu, Zheng
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Berlin, Aaron A
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White, Natalie
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show more...
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Mori, Michiko
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Pham, Tuyet-Hang
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Ward, Christine ...
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Criner, Gerard J
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Marchetti, Natha ...
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Mustelin, Tomas
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Erjefält, Jonas
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Kolbeck, Roland
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Humbles, Alison ...
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show less...
- About the subject
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- MEDICAL AND HEALTH SCIENCES
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MEDICAL AND HEAL ...
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and Basic Medicine
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and Immunology in th ...
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Immunity
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Lund University