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Interleukin-17 regulation: an attractive therapeutic approach for asthma
Interleukin (IL)-17 is recognized to play a critical role in numerous immune and inflammatory responses by regulating the expression of various inflammatory mediators, which include cytokines, chemokines, and adhesion molecules. There is growing evidence that IL-17 is involved in the pathogenesis of...
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2010
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2894770/ https://www.ncbi.nlm.nih.gov/pubmed/20565710 http://dx.doi.org/10.1186/1465-9921-11-78 |
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author | Park, Seoung Ju Lee, Yong Chul |
author_facet | Park, Seoung Ju Lee, Yong Chul |
author_sort | Park, Seoung Ju |
collection | PubMed |
description | Interleukin (IL)-17 is recognized to play a critical role in numerous immune and inflammatory responses by regulating the expression of various inflammatory mediators, which include cytokines, chemokines, and adhesion molecules. There is growing evidence that IL-17 is involved in the pathogenesis of asthma. IL-17 orchestrates the neutrophilic influx into the airways and also enhances T-helper 2 (Th2) cell-mediated eosinophilic airway inflammation in asthma. Recent studies have demonstrated that not only inhibitor of IL-17 per se but also diverse regulators of IL-17 expression reduce antigen-induced airway inflammation, bronchial hyperresponsiveness, and Th2 cytokine levels in animal models of asthma. This review will summarize the role of IL-17 in the context of allergic airway inflammation and discuss the therapeutic potential of various strategies targeting IL-17 for asthma. |
format | Text |
id | pubmed-2894770 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2010 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-28947702010-07-01 Interleukin-17 regulation: an attractive therapeutic approach for asthma Park, Seoung Ju Lee, Yong Chul Respir Res Review Interleukin (IL)-17 is recognized to play a critical role in numerous immune and inflammatory responses by regulating the expression of various inflammatory mediators, which include cytokines, chemokines, and adhesion molecules. There is growing evidence that IL-17 is involved in the pathogenesis of asthma. IL-17 orchestrates the neutrophilic influx into the airways and also enhances T-helper 2 (Th2) cell-mediated eosinophilic airway inflammation in asthma. Recent studies have demonstrated that not only inhibitor of IL-17 per se but also diverse regulators of IL-17 expression reduce antigen-induced airway inflammation, bronchial hyperresponsiveness, and Th2 cytokine levels in animal models of asthma. This review will summarize the role of IL-17 in the context of allergic airway inflammation and discuss the therapeutic potential of various strategies targeting IL-17 for asthma. BioMed Central 2010 2010-06-16 /pmc/articles/PMC2894770/ /pubmed/20565710 http://dx.doi.org/10.1186/1465-9921-11-78 Text en Copyright ©2010 Park and Lee; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Park, Seoung Ju Lee, Yong Chul Interleukin-17 regulation: an attractive therapeutic approach for asthma |
title | Interleukin-17 regulation: an attractive therapeutic approach for asthma |
title_full | Interleukin-17 regulation: an attractive therapeutic approach for asthma |
title_fullStr | Interleukin-17 regulation: an attractive therapeutic approach for asthma |
title_full_unstemmed | Interleukin-17 regulation: an attractive therapeutic approach for asthma |
title_short | Interleukin-17 regulation: an attractive therapeutic approach for asthma |
title_sort | interleukin-17 regulation: an attractive therapeutic approach for asthma |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2894770/ https://www.ncbi.nlm.nih.gov/pubmed/20565710 http://dx.doi.org/10.1186/1465-9921-11-78 |
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