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IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models
Previous studies have shown that IL-22, one of the Th17 cell–related cytokines, plays multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 cells; however, the underlying mechanism remains unclear. Here, we show that allergic airway inflammation and Th2 and Th17 cy...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5626396/ https://www.ncbi.nlm.nih.gov/pubmed/28811323 http://dx.doi.org/10.1084/jem.20162108 |
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author | Ito, Takashi Hirose, Koichi Saku, Aiko Kono, Kenta Takatori, Hiroaki Tamachi, Tomohiro Goto, Yoshiyuki Renauld, Jean-Christophe Kiyono, Hiroshi Nakajima, Hiroshi |
author_facet | Ito, Takashi Hirose, Koichi Saku, Aiko Kono, Kenta Takatori, Hiroaki Tamachi, Tomohiro Goto, Yoshiyuki Renauld, Jean-Christophe Kiyono, Hiroshi Nakajima, Hiroshi |
author_sort | Ito, Takashi |
collection | PubMed |
description | Previous studies have shown that IL-22, one of the Th17 cell–related cytokines, plays multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 cells; however, the underlying mechanism remains unclear. Here, we show that allergic airway inflammation and Th2 and Th17 cytokine production upon intratracheal administration of house dust mite (HDM) extract, a representative allergen, were exacerbated in IL-22-deficient mice. We also found that IL-22 induces Reg3γ production from lung epithelial cells through STAT3 activation and that neutralization of Reg3γ significantly exacerbates HDM-induced eosinophilic airway inflammation and Th2 cytokine induction. Moreover, exostatin-like 3 (EXTL3), a functional Reg3γ binding protein, is expressed in lung epithelial cells, and intratracheal administration of recombinant Reg3γ suppresses HDM-induced thymic stromal lymphopoietin and IL-33 expression and accumulation of type 2 innate lymphoid cells in the lung. Collectively, these results suggest that IL-22 induces Reg3γ production from lung epithelial cells and inhibits the development of HDM-induced allergic airway inflammation, possibly by inhibiting cytokine production from lung epithelial cells. |
format | Online Article Text |
id | pubmed-5626396 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-56263962018-04-02 IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models Ito, Takashi Hirose, Koichi Saku, Aiko Kono, Kenta Takatori, Hiroaki Tamachi, Tomohiro Goto, Yoshiyuki Renauld, Jean-Christophe Kiyono, Hiroshi Nakajima, Hiroshi J Exp Med Research Articles Previous studies have shown that IL-22, one of the Th17 cell–related cytokines, plays multiple roles in regulating allergic airway inflammation caused by antigen-specific Th2 cells; however, the underlying mechanism remains unclear. Here, we show that allergic airway inflammation and Th2 and Th17 cytokine production upon intratracheal administration of house dust mite (HDM) extract, a representative allergen, were exacerbated in IL-22-deficient mice. We also found that IL-22 induces Reg3γ production from lung epithelial cells through STAT3 activation and that neutralization of Reg3γ significantly exacerbates HDM-induced eosinophilic airway inflammation and Th2 cytokine induction. Moreover, exostatin-like 3 (EXTL3), a functional Reg3γ binding protein, is expressed in lung epithelial cells, and intratracheal administration of recombinant Reg3γ suppresses HDM-induced thymic stromal lymphopoietin and IL-33 expression and accumulation of type 2 innate lymphoid cells in the lung. Collectively, these results suggest that IL-22 induces Reg3γ production from lung epithelial cells and inhibits the development of HDM-induced allergic airway inflammation, possibly by inhibiting cytokine production from lung epithelial cells. The Rockefeller University Press 2017-10-02 /pmc/articles/PMC5626396/ /pubmed/28811323 http://dx.doi.org/10.1084/jem.20162108 Text en © 2017 Ito et al. http://www.rupress.org/terms/https://creativecommons.org/licenses/by-nc-sa/4.0/This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/). |
spellingShingle | Research Articles Ito, Takashi Hirose, Koichi Saku, Aiko Kono, Kenta Takatori, Hiroaki Tamachi, Tomohiro Goto, Yoshiyuki Renauld, Jean-Christophe Kiyono, Hiroshi Nakajima, Hiroshi IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models |
title | IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models |
title_full | IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models |
title_fullStr | IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models |
title_full_unstemmed | IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models |
title_short | IL-22 induces Reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models |
title_sort | il-22 induces reg3γ and inhibits allergic inflammation in house dust mite–induced asthma models |
topic | Research Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5626396/ https://www.ncbi.nlm.nih.gov/pubmed/28811323 http://dx.doi.org/10.1084/jem.20162108 |
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