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Maintenance of memory-type pathogenic Th2 cells in the pathophysiology of chronic airway inflammation
BACKGROUND: Immunological memory is critical for long-standing protection against microorganisms; however, certain antigen-specific memory CD4(+) T helper (Th) cells drive immune-related pathology, including chronic allergic inflammation such as asthma. The IL-5-producing memory-type Tpath2 subset i...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6009957/ https://www.ncbi.nlm.nih.gov/pubmed/29951134 http://dx.doi.org/10.1186/s41232-018-0067-8 |
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author | Hirahara, Kiyoshi Shinoda, Kenta Endo, Yusuke Ichikawa, Tomomi Nakayama, Toshinori |
author_facet | Hirahara, Kiyoshi Shinoda, Kenta Endo, Yusuke Ichikawa, Tomomi Nakayama, Toshinori |
author_sort | Hirahara, Kiyoshi |
collection | PubMed |
description | BACKGROUND: Immunological memory is critical for long-standing protection against microorganisms; however, certain antigen-specific memory CD4(+) T helper (Th) cells drive immune-related pathology, including chronic allergic inflammation such as asthma. The IL-5-producing memory-type Tpath2 subset is important for the pathogenesis of chronic allergic inflammation. This memory-type pathogenic Th2 cell population (Tpath2) can be detected in various allergic inflammatory lesions. However, how these pathogenic populations are maintained at the local inflammatory site has remained unclear. METHODS: We performed a series of experiments using mice model for chronic airway inflammation. We also investigated the human samples from patients with eosinophilic chronic rhinosinusitis. RESULTS: We recently reported that inducible bronchus-associated lymphoid tissue (iBALT) was shaped during chronic inflammation in the lung. We also found that memory-type Tpath2 cells are maintained within iBALT. The maintenance of the Tpath2 cells within iBALT is supported by specific cell subpopulations within the lung. Furthermore, ectopic lymphoid structures consisting of memory CD4(+) T cells were found in nasal polyps of eosinophilic chronic rhinosinusitis patients, indicating that the persistence of inflammation is controlled by these structures. CONCLUSION: Thus, the cell components that organize iBALT formation may be therapeutic targets for chronic allergic airway inflammation. |
format | Online Article Text |
id | pubmed-6009957 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-60099572018-06-27 Maintenance of memory-type pathogenic Th2 cells in the pathophysiology of chronic airway inflammation Hirahara, Kiyoshi Shinoda, Kenta Endo, Yusuke Ichikawa, Tomomi Nakayama, Toshinori Inflamm Regen Review BACKGROUND: Immunological memory is critical for long-standing protection against microorganisms; however, certain antigen-specific memory CD4(+) T helper (Th) cells drive immune-related pathology, including chronic allergic inflammation such as asthma. The IL-5-producing memory-type Tpath2 subset is important for the pathogenesis of chronic allergic inflammation. This memory-type pathogenic Th2 cell population (Tpath2) can be detected in various allergic inflammatory lesions. However, how these pathogenic populations are maintained at the local inflammatory site has remained unclear. METHODS: We performed a series of experiments using mice model for chronic airway inflammation. We also investigated the human samples from patients with eosinophilic chronic rhinosinusitis. RESULTS: We recently reported that inducible bronchus-associated lymphoid tissue (iBALT) was shaped during chronic inflammation in the lung. We also found that memory-type Tpath2 cells are maintained within iBALT. The maintenance of the Tpath2 cells within iBALT is supported by specific cell subpopulations within the lung. Furthermore, ectopic lymphoid structures consisting of memory CD4(+) T cells were found in nasal polyps of eosinophilic chronic rhinosinusitis patients, indicating that the persistence of inflammation is controlled by these structures. CONCLUSION: Thus, the cell components that organize iBALT formation may be therapeutic targets for chronic allergic airway inflammation. BioMed Central 2018-06-20 /pmc/articles/PMC6009957/ /pubmed/29951134 http://dx.doi.org/10.1186/s41232-018-0067-8 Text en © The Author(s) 2018 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Review Hirahara, Kiyoshi Shinoda, Kenta Endo, Yusuke Ichikawa, Tomomi Nakayama, Toshinori Maintenance of memory-type pathogenic Th2 cells in the pathophysiology of chronic airway inflammation |
title | Maintenance of memory-type pathogenic Th2 cells in the pathophysiology of chronic airway inflammation |
title_full | Maintenance of memory-type pathogenic Th2 cells in the pathophysiology of chronic airway inflammation |
title_fullStr | Maintenance of memory-type pathogenic Th2 cells in the pathophysiology of chronic airway inflammation |
title_full_unstemmed | Maintenance of memory-type pathogenic Th2 cells in the pathophysiology of chronic airway inflammation |
title_short | Maintenance of memory-type pathogenic Th2 cells in the pathophysiology of chronic airway inflammation |
title_sort | maintenance of memory-type pathogenic th2 cells in the pathophysiology of chronic airway inflammation |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6009957/ https://www.ncbi.nlm.nih.gov/pubmed/29951134 http://dx.doi.org/10.1186/s41232-018-0067-8 |
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