Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.

Respiratory syncytial virus (RSV) infection is the leading viral cause of severe lower respiratory tract illness in young infants. Clinical studies have documented that certain polymorphisms in the gene encoding the regulatory cytokine IL-10 are associated with the development of severe bronchioliti...

Descripción completa

Guardado en:
Detalles Bibliográficos
Autores principales: Jie Sun, Amber Cardani, Ashish K Sharma, Victor E Laubach, Robert S Jack, Werner Müller, Thomas J Braciale
Formato: article
Lenguaje:EN
Publicado: Public Library of Science (PLoS) 2011
Materias:
Acceso en línea:https://doaj.org/article/1f3bc5482d2d41dda44d7e4b8b97680a
Etiquetas: Agregar Etiqueta
Sin Etiquetas, Sea el primero en etiquetar este registro!
id oai:doaj.org-article:1f3bc5482d2d41dda44d7e4b8b97680a
record_format dspace
spelling oai:doaj.org-article:1f3bc5482d2d41dda44d7e4b8b97680a2021-11-18T06:03:08ZAutocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.1553-73661553-737410.1371/journal.ppat.1002173https://doaj.org/article/1f3bc5482d2d41dda44d7e4b8b97680a2011-08-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21829368/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Respiratory syncytial virus (RSV) infection is the leading viral cause of severe lower respiratory tract illness in young infants. Clinical studies have documented that certain polymorphisms in the gene encoding the regulatory cytokine IL-10 are associated with the development of severe bronchiolitis in RSV infected infants. Here, we examined the role of IL-10 in a murine model of primary RSV infection and found that high levels of IL-10 are produced in the respiratory tract by anti-viral effector T cells at the onset of the adaptive immune response. We demonstrated that the function of the effector T cell -derived IL-10 in vivo is to limit the excess pulmonary inflammation and thereby to maintain critical lung function. We further identify a novel mechanism by which effector T cell-derived IL-10 controls excess inflammation by feedback inhibition through engagement of the IL-10 receptor on the antiviral effector T cells. Our findings suggest a potentially critical role of effector T cell-derived IL-10 in controlling disease severity in clinical RSV infection.Jie SunAmber CardaniAshish K SharmaVictor E LaubachRobert S JackWerner MüllerThomas J BracialePublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 7, Iss 8, p e1002173 (2011)
institution DOAJ
collection DOAJ
language EN
topic Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
spellingShingle Immunologic diseases. Allergy
RC581-607
Biology (General)
QH301-705.5
Jie Sun
Amber Cardani
Ashish K Sharma
Victor E Laubach
Robert S Jack
Werner Müller
Thomas J Braciale
Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.
description Respiratory syncytial virus (RSV) infection is the leading viral cause of severe lower respiratory tract illness in young infants. Clinical studies have documented that certain polymorphisms in the gene encoding the regulatory cytokine IL-10 are associated with the development of severe bronchiolitis in RSV infected infants. Here, we examined the role of IL-10 in a murine model of primary RSV infection and found that high levels of IL-10 are produced in the respiratory tract by anti-viral effector T cells at the onset of the adaptive immune response. We demonstrated that the function of the effector T cell -derived IL-10 in vivo is to limit the excess pulmonary inflammation and thereby to maintain critical lung function. We further identify a novel mechanism by which effector T cell-derived IL-10 controls excess inflammation by feedback inhibition through engagement of the IL-10 receptor on the antiviral effector T cells. Our findings suggest a potentially critical role of effector T cell-derived IL-10 in controlling disease severity in clinical RSV infection.
format article
author Jie Sun
Amber Cardani
Ashish K Sharma
Victor E Laubach
Robert S Jack
Werner Müller
Thomas J Braciale
author_facet Jie Sun
Amber Cardani
Ashish K Sharma
Victor E Laubach
Robert S Jack
Werner Müller
Thomas J Braciale
author_sort Jie Sun
title Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.
title_short Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.
title_full Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.
title_fullStr Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.
title_full_unstemmed Autocrine regulation of pulmonary inflammation by effector T-cell derived IL-10 during infection with respiratory syncytial virus.
title_sort autocrine regulation of pulmonary inflammation by effector t-cell derived il-10 during infection with respiratory syncytial virus.
publisher Public Library of Science (PLoS)
publishDate 2011
url https://doaj.org/article/1f3bc5482d2d41dda44d7e4b8b97680a
work_keys_str_mv AT jiesun autocrineregulationofpulmonaryinflammationbyeffectortcellderivedil10duringinfectionwithrespiratorysyncytialvirus
AT ambercardani autocrineregulationofpulmonaryinflammationbyeffectortcellderivedil10duringinfectionwithrespiratorysyncytialvirus
AT ashishksharma autocrineregulationofpulmonaryinflammationbyeffectortcellderivedil10duringinfectionwithrespiratorysyncytialvirus
AT victorelaubach autocrineregulationofpulmonaryinflammationbyeffectortcellderivedil10duringinfectionwithrespiratorysyncytialvirus
AT robertsjack autocrineregulationofpulmonaryinflammationbyeffectortcellderivedil10duringinfectionwithrespiratorysyncytialvirus
AT wernermuller autocrineregulationofpulmonaryinflammationbyeffectortcellderivedil10duringinfectionwithrespiratorysyncytialvirus
AT thomasjbraciale autocrineregulationofpulmonaryinflammationbyeffectortcellderivedil10duringinfectionwithrespiratorysyncytialvirus
_version_ 1718424653001654272