Modeling T<inf>H</inf>2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma

Foster, PS; Maltby, S; Rosenberg, HF; Tay, HL; Hogan, SP; Collison, AM; Yang, M; Kaiko, GE; Hansbro, PM; Kumar, RK; Mattes, J

Modeling T<inf>H</inf>2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma

Foster, PS Maltby, S Rosenberg, HF Tay, HL Hogan, SP Collison, AM Yang, M Kaiko, GE Hansbro, PM

Kumar, RK Mattes, J

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Publication Type:: Journal Article
Citation:: Immunological Reviews, 2017, 278 (1), pp. 20 - 40
Issue Date:: 2017-07-01

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Field	Value	Language
dc.contributor.author	Foster, PS	en_US
dc.contributor.author	Maltby, S	en_US
dc.contributor.author	Rosenberg, HF	en_US
dc.contributor.author	Tay, HL	en_US
dc.contributor.author	Hogan, SP	en_US
dc.contributor.author	Collison, AM	en_US
dc.contributor.author	Yang, M	en_US
dc.contributor.author	Kaiko, GE	en_US
dc.contributor.author	Hansbro, PM https://orcid.org/0000-0002-4741-3035	en_US
dc.contributor.author	Kumar, RK	en_US
dc.contributor.author	Mattes, J	en_US
dc.date.available	2017-02-25	en_US
dc.date.issued	2017-07-01	en_US
dc.identifier.citation	Immunological Reviews, 2017, 278 (1), pp. 20 - 40	en_US
dc.identifier.issn	0105-2896	en_US
dc.identifier.uri	http://hdl.handle.net/10453/126243
dc.description.abstract	© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd In this review, we highlight experiments conducted in our laboratories that have elucidated functional roles for CD4+ T-helper type-2 lymphocytes (TH2 cells), their associated cytokines, and eosinophils in the regulation of hallmark features of allergic asthma. Notably, we consider the complexity of type-2 responses and studies that have explored integrated signaling among classical TH2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (AHR). Among our most important findings, we have provided evidence that the initiation of TH2 responses is regulated by airway epithelial cell-derived factors, including TRAIL and MID1, which promote TH2 cell development via STAT6-dependent pathways. Further, we highlight studies demonstrating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inflammatory therapy. On the background of TH2 inflammation, we have demonstrated that innate immune cells (notably, airway macrophages) play essential roles in the generation of steroid-resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerbations. Our work clearly indicates that understanding the diversity and spatiotemporal role of the inflammatory response and its interactions with resident airway cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeutic approaches.	en_US
dc.relation.ispartof	Immunological Reviews	en_US
dc.relation.isbasedon	10.1111/imr.12549	en_US
dc.subject.classification	Immunology	en_US
dc.subject.mesh	T-Lymphocyte Subsets	en_US
dc.subject.mesh	Th2 Cells	en_US
dc.subject.mesh	Immune System	en_US
dc.subject.mesh	Animals	en_US
dc.subject.mesh	Humans	en_US
dc.subject.mesh	Asthma	en_US
dc.subject.mesh	Respiratory Hypersensitivity	en_US
dc.subject.mesh	Disease Susceptibility	en_US
dc.subject.mesh	Immunoglobulin E	en_US
dc.subject.mesh	MicroRNAs	en_US
dc.subject.mesh	Anti-Asthmatic Agents	en_US
dc.subject.mesh	Antibodies, Anti-Idiotypic	en_US
dc.subject.mesh	Cytokines	en_US
dc.subject.mesh	Cell Communication	en_US
dc.subject.mesh	Signal Transduction	en_US
dc.subject.mesh	Drug Resistance	en_US
dc.subject.mesh	Models, Biological	en_US
dc.subject.mesh	Chemokine CCL11	en_US
dc.subject.mesh	Immunomodulation	en_US
dc.title	Modeling T<inf>H</inf>2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma	en_US
dc.type	Journal Article
utslib.citation.volume	1	en_US
utslib.citation.volume	278	en_US
utslib.for	1107 Immunology	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	278	en_US

Abstract:

© 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd In this review, we highlight experiments conducted in our laboratories that have elucidated functional roles for CD4+ T-helper type-2 lymphocytes (TH2 cells), their associated cytokines, and eosinophils in the regulation of hallmark features of allergic asthma. Notably, we consider the complexity of type-2 responses and studies that have explored integrated signaling among classical TH2 cytokines (IL-4, IL-5, and IL-13), which together with CCL11 (eotaxin-1) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper-responsiveness (AHR). Among our most important findings, we have provided evidence that the initiation of TH2 responses is regulated by airway epithelial cell-derived factors, including TRAIL and MID1, which promote TH2 cell development via STAT6-dependent pathways. Further, we highlight studies demonstrating that microRNAs are key regulators of allergic inflammation and potential targets for anti-inflammatory therapy. On the background of TH2 inflammation, we have demonstrated that innate immune cells (notably, airway macrophages) play essential roles in the generation of steroid-resistant inflammation and AHR secondary to allergen- and pathogen-induced exacerbations. Our work clearly indicates that understanding the diversity and spatiotemporal role of the inflammatory response and its interactions with resident airway cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeutic approaches.

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http://hdl.handle.net/10453/126243