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
- Publication Type:
- Journal Article
- Citation:
- Immunological Reviews, 2017, 278 (1), pp. 20 - 40
- Issue Date:
- 2017-07-01
Closed Access
Full metadata record
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 |
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.subject.mesh | Animals | en_US |
dc.subject.mesh | Anti-Asthmatic Agents | en_US |
dc.subject.mesh | Antibodies, Anti-Idiotypic | en_US |
dc.subject.mesh | Asthma | en_US |
dc.subject.mesh | Cell Communication | en_US |
dc.subject.mesh | Chemokine CCL11 | en_US |
dc.subject.mesh | Cytokines | en_US |
dc.subject.mesh | Disease Susceptibility | en_US |
dc.subject.mesh | Drug Resistance | en_US |
dc.subject.mesh | Humans | en_US |
dc.subject.mesh | Immune System | en_US |
dc.subject.mesh | Immunoglobulin E | en_US |
dc.subject.mesh | Immunomodulation | en_US |
dc.subject.mesh | MicroRNAs | en_US |
dc.subject.mesh | Models, Biological | en_US |
dc.subject.mesh | Respiratory Hypersensitivity | en_US |
dc.subject.mesh | Signal Transduction | en_US |
dc.subject.mesh | T-Lymphocyte Subsets | en_US |
dc.subject.mesh | Th2 Cells | 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.description.version | Published | en_US |
utslib.citation.volume | 1 | en_US |
utslib.citation.volume | 278 | en_US |
utslib.for | 1107 Immunology | 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 | |
utslib.copyright.status | closed_access | |
pubs.issue | 1 | en_US |
pubs.publication-status | Published | en_US |
pubs.volume | 278 | en_US |
Files in This Item:
Filename | Description | Size | |||
---|---|---|---|---|---|
Foster_et_al-2017-Immunological_Reviews.pdf | Published Version | 788.08 kB | Adobe PDF |
Copyright Clearance Process
- Recently Added
- In Progress
- Closed Access
This item is closed access and not available.
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.
Please use this identifier to cite or link to this item: