Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease

Donovan, C; Starkey, MR; Kim, RY; Rana, BMJ; Barlow, JL; Jones, B; Haw, TJ; Mono Nair, P; Budden, K; Cameron, GJM; Horvat, JC; Wark, PA; Foster, PS; McKenzie, ANJ; Hansbro, PM

Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease

Donovan, C Starkey, MR Kim, RY

Rana, BMJ Barlow, JL Jones, B Haw, TJ Mono Nair, P Budden, K Cameron, GJM Horvat, JC Wark, PA Foster, PS McKenzie, ANJ Hansbro, PM

Permalink

Publication Type:: Journal Article
Citation:: Journal of Leukocyte Biology, 2019, 105 (1), pp. 143 - 150
Issue Date:: 2019-01-01

Closed Access

	Filename	Description	Size
	Donovan_et_al-2019-Journal_of_Leukocyte_Biology.pdf	Published Version	1.67 MB	Adobe PDF	View/Open

Copyright Clearance Process

Recently Added
In Progress
Closed Access

This item is closed access and not available.

Full metadata record

Field	Value	Language
dc.contributor.author	Donovan, C	en_US
dc.contributor.author	Starkey, MR	en_US
dc.contributor.author	Kim, RY https://orcid.org/0000-0002-8709-5270	en_US
dc.contributor.author	Rana, BMJ	en_US
dc.contributor.author	Barlow, JL	en_US
dc.contributor.author	Jones, B	en_US
dc.contributor.author	Haw, TJ	en_US
dc.contributor.author	Mono Nair, P	en_US
dc.contributor.author	Budden, K	en_US
dc.contributor.author	Cameron, GJM	en_US
dc.contributor.author	Horvat, JC	en_US
dc.contributor.author	Wark, PA	en_US
dc.contributor.author	Foster, PS	en_US
dc.contributor.author	McKenzie, ANJ	en_US
dc.contributor.author	Hansbro, PM https://orcid.org/0000-0002-4741-3035	en_US
dc.date.available	2018-08-14	en_US
dc.date.issued	2019-01-01	en_US
dc.identifier.citation	Journal of Leukocyte Biology, 2019, 105 (1), pp. 143 - 150	en_US
dc.identifier.issn	0741-5400	en_US
dc.identifier.uri	http://hdl.handle.net/10453/130991
dc.description.abstract	©2018 Society for Leukocyte Biology Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogenesis of COPD are unclear. Therefore, we investigated the roles of T and B lymphocytes and group 2 innate lymphoid cells (ILC2s) in airway inflammation and remodelling, and lung function in an experimental model of COPD using mice that specifically lack these cells (Rag1 −/− and Rora fl/fl Il7r Cre [ILC2-deficient] mice). Wild-type (WT) C57BL/6 mice, Rag1 −/− , and Rora fl/fl Il7r Cre mice were exposed to cigarette smoke (CS; 12 cigarettes twice a day, 5 days a week) for up to 12 weeks, and airway inflammation, airway remodelling (collagen deposition and alveolar enlargement), and lung function were assessed. WT, Rag1 −/− , and ILC2-deficient mice exposed to CS had similar levels of airway inflammation and impaired lung function. CS exposure increased small airway collagen deposition in WT mice. Rag1 −/− normal air- and CS-exposed mice had significantly increased collagen deposition compared to similarly exposed WT mice, which was associated with increases in IL-33, IL-13, and ILC2 numbers. CS-exposed Rora fl/fl Il7r Cre mice were protected from emphysema, but had increased IL-33/IL-13 expression and collagen deposition compared to WT CS-exposed mice. T/B lymphocytes and ILC2s play roles in airway collagen deposition/fibrosis, but not inflammation, in experimental COPD.	en_US
dc.relation	http://purl.org/au-research/grants/nhmrc/GNT1079187
dc.relation.ispartof	Journal of Leukocyte Biology	en_US
dc.relation.isbasedon	10.1002/JLB.3AB0518-178R	en_US
dc.subject.classification	Immunology	en_US
dc.subject.mesh	Pulmonary Alveoli	en_US
dc.subject.mesh	B-Lymphocytes	en_US
dc.subject.mesh	T-Lymphocytes	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Mice, Inbred C57BL	en_US
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive	en_US
dc.subject.mesh	Pneumonia	en_US
dc.subject.mesh	Respiratory Hypersensitivity	en_US
dc.subject.mesh	Body Weight	en_US
dc.subject.mesh	Collagen	en_US
dc.subject.mesh	Homeodomain Proteins	en_US
dc.subject.mesh	Interleukins	en_US
dc.subject.mesh	Airway Resistance	en_US
dc.subject.mesh	Cell Count	en_US
dc.subject.mesh	Immunity, Innate	en_US
dc.subject.mesh	Airway Remodeling	en_US
dc.title	Roles for T/B lymphocytes and ILC2s in experimental chronic obstructive pulmonary disease	en_US
dc.type	Journal Article
utslib.citation.volume	1	en_US
utslib.citation.volume	105	en_US
utslib.for	1107 Immunology	en_US
utslib.for	0601 Biochemistry and Cell Biology	en_US
pubs.embargo.period	Not known	en_US
pubs.organisational-group	/University of Technology Sydney
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney/Faculty of Science/School of Life Sciences
utslib.copyright.status	closed_access
pubs.issue	1	en_US
pubs.publication-status	Published	en_US
pubs.volume	105	en_US

Abstract:

©2018 Society for Leukocyte Biology Pulmonary inflammation in chronic obstructive pulmonary disease (COPD) is characterized by both innate and adaptive immune responses; however, their specific roles in the pathogenesis of COPD are unclear. Therefore, we investigated the roles of T and B lymphocytes and group 2 innate lymphoid cells (ILC2s) in airway inflammation and remodelling, and lung function in an experimental model of COPD using mice that specifically lack these cells (Rag1 −/− and Rora fl/fl Il7r Cre [ILC2-deficient] mice). Wild-type (WT) C57BL/6 mice, Rag1 −/− , and Rora fl/fl Il7r Cre mice were exposed to cigarette smoke (CS; 12 cigarettes twice a day, 5 days a week) for up to 12 weeks, and airway inflammation, airway remodelling (collagen deposition and alveolar enlargement), and lung function were assessed. WT, Rag1 −/− , and ILC2-deficient mice exposed to CS had similar levels of airway inflammation and impaired lung function. CS exposure increased small airway collagen deposition in WT mice. Rag1 −/− normal air- and CS-exposed mice had significantly increased collagen deposition compared to similarly exposed WT mice, which was associated with increases in IL-33, IL-13, and ILC2 numbers. CS-exposed Rora fl/fl Il7r Cre mice were protected from emphysema, but had increased IL-33/IL-13 expression and collagen deposition compared to WT CS-exposed mice. T/B lymphocytes and ILC2s play roles in airway collagen deposition/fibrosis, but not inflammation, in experimental COPD.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/130991