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Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation
Airborne exposure to microbial cell wall lipids such as lipopolysaccharide triggers innate immune responses that regulate susceptibility to allergic airway inflammation. α-Glycosylceramides represent another widespread class of microbial lipids that directly stimulate innate-like, IL-4– and IL-13–pr...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Rockefeller University Press
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182052/ https://www.ncbi.nlm.nih.gov/pubmed/21930768 http://dx.doi.org/10.1084/jem.20110522 |
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author | Scanlon, Seth T. Thomas, Seddon Y. Ferreira, Caroline M. Bai, Li Krausz, Thomas Savage, Paul B. Bendelac, Albert |
author_facet | Scanlon, Seth T. Thomas, Seddon Y. Ferreira, Caroline M. Bai, Li Krausz, Thomas Savage, Paul B. Bendelac, Albert |
author_sort | Scanlon, Seth T. |
collection | PubMed |
description | Airborne exposure to microbial cell wall lipids such as lipopolysaccharide triggers innate immune responses that regulate susceptibility to allergic airway inflammation. α-Glycosylceramides represent another widespread class of microbial lipids that directly stimulate innate-like, IL-4– and IL-13–producing, CD1d-restricted NKT cells. In this study, we demonstrate that NKT cells constitutively accumulate and reside in the microvasculature of the mouse lung. After a single airborne exposure to lipid antigen, they promptly extravasate to orchestrate the formation of peribronchiolar and interstitial lymphohistiocytic granulomas containing numerous eosinophils. Concomitant airborne exposure to ovalbumin (OVA) induces the priming of OVA-specific Th2 cells and IgE antibodies by the same dendritic cell coexpressing CD1d and MHC class II. Although NKT cell activation remains confined to the lipid-exposed lung and draining lymph nodes, Th2 cells recirculate and seed the lung of a parabiotic partner, conferring susceptibility to OVA challenge months after the initial exposure, in a manner independent of NKT cells and CD1d. Thus, transient recruitment and activation of lung-resident intravascular NKT cells can trigger long-term susceptibility to allergic airway inflammation. |
format | Online Article Text |
id | pubmed-3182052 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | The Rockefeller University Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-31820522012-03-26 Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation Scanlon, Seth T. Thomas, Seddon Y. Ferreira, Caroline M. Bai, Li Krausz, Thomas Savage, Paul B. Bendelac, Albert J Exp Med Article Airborne exposure to microbial cell wall lipids such as lipopolysaccharide triggers innate immune responses that regulate susceptibility to allergic airway inflammation. α-Glycosylceramides represent another widespread class of microbial lipids that directly stimulate innate-like, IL-4– and IL-13–producing, CD1d-restricted NKT cells. In this study, we demonstrate that NKT cells constitutively accumulate and reside in the microvasculature of the mouse lung. After a single airborne exposure to lipid antigen, they promptly extravasate to orchestrate the formation of peribronchiolar and interstitial lymphohistiocytic granulomas containing numerous eosinophils. Concomitant airborne exposure to ovalbumin (OVA) induces the priming of OVA-specific Th2 cells and IgE antibodies by the same dendritic cell coexpressing CD1d and MHC class II. Although NKT cell activation remains confined to the lipid-exposed lung and draining lymph nodes, Th2 cells recirculate and seed the lung of a parabiotic partner, conferring susceptibility to OVA challenge months after the initial exposure, in a manner independent of NKT cells and CD1d. Thus, transient recruitment and activation of lung-resident intravascular NKT cells can trigger long-term susceptibility to allergic airway inflammation. The Rockefeller University Press 2011-09-26 /pmc/articles/PMC3182052/ /pubmed/21930768 http://dx.doi.org/10.1084/jem.20110522 Text en © 2011 Scanlon et al. 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 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/). |
spellingShingle | Article Scanlon, Seth T. Thomas, Seddon Y. Ferreira, Caroline M. Bai, Li Krausz, Thomas Savage, Paul B. Bendelac, Albert Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation |
title | Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation |
title_full | Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation |
title_fullStr | Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation |
title_full_unstemmed | Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation |
title_short | Airborne lipid antigens mobilize resident intravascular NKT cells to induce allergic airway inflammation |
title_sort | airborne lipid antigens mobilize resident intravascular nkt cells to induce allergic airway inflammation |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3182052/ https://www.ncbi.nlm.nih.gov/pubmed/21930768 http://dx.doi.org/10.1084/jem.20110522 |
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