Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Scanlon, Seth T., Thomas, Seddon Y., Ferreira, Caroline M., Bai, Li, Krausz, Thomas, Savage, Paul B., Bendelac, Albert
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2011
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
_version_ 1782212862715887616
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
work_keys_str_mv AT scanlonsetht airbornelipidantigensmobilizeresidentintravascularnktcellstoinduceallergicairwayinflammation
AT thomasseddony airbornelipidantigensmobilizeresidentintravascularnktcellstoinduceallergicairwayinflammation
AT ferreiracarolinem airbornelipidantigensmobilizeresidentintravascularnktcellstoinduceallergicairwayinflammation
AT baili airbornelipidantigensmobilizeresidentintravascularnktcellstoinduceallergicairwayinflammation
AT krauszthomas airbornelipidantigensmobilizeresidentintravascularnktcellstoinduceallergicairwayinflammation
AT savagepaulb airbornelipidantigensmobilizeresidentintravascularnktcellstoinduceallergicairwayinflammation
AT bendelacalbert airbornelipidantigensmobilizeresidentintravascularnktcellstoinduceallergicairwayinflammation