Show simple item record

dc.contributor.authorMathews, Joel A.en_US
dc.contributor.authorWilliams, Alison S.en_US
dc.contributor.authorBrand, Jeffrey D.en_US
dc.contributor.authorWurmbrand, Allison P.en_US
dc.contributor.authorChen, Lucasen_US
dc.contributor.authorNinin, Fernanda MC.en_US
dc.contributor.authorSi, Huiqingen_US
dc.contributor.authorKasahara, David I.en_US
dc.contributor.authorShore, Stephanie A.en_US
dc.date.accessioned2014-07-07T18:13:23Z
dc.date.issued2014en_US
dc.identifier.citationMathews, Joel A., Alison S. Williams, Jeffrey D. Brand, Allison P. Wurmbrand, Lucas Chen, Fernanda MC. Ninin, Huiqing Si, David I. Kasahara, and Stephanie A. Shore. 2014. “γδ T Cells Are Required for Pulmonary IL-17A Expression after Ozone Exposure in Mice: Role of TNFα.” PLoS ONE 9 (5): e97707. doi:10.1371/journal.pone.0097707. http://dx.doi.org/10.1371/journal.pone.0097707.en
dc.identifier.issn1932-6203en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:12406878
dc.description.abstractOzone is an air pollutant that causes pulmonary symptoms. In mice, ozone exposure causes pulmonary injury and increases bronchoalveolar lavage macrophages and neutrophils. We have shown that IL-17A is important in the recruitment of neutrophils after subacute ozone exposure (0.3 ppm for 24–72 h). We hypothesized that γδ T cells are the main producers of IL-17A after subacute ozone. To explore this hypothesis we exposed wildtype mice and mice deficient in γδ T cells (TCRδ−/−) to ozone or room air. Ozone-induced increases in BAL macrophages and neutrophils were attenuated in TCRδ−/− mice. Ozone increased the number of γδ T cells in the lungs and increased pulmonary Il17a mRNA expression and the number of IL-17A+ CD45+ cells in the lungs and these effects were abolished in TCRδ−/− mice. Ozone-induced increases in factors downstream of IL-17A signaling, including G-CSF, IL-6, IP-10 and KC were also decreased in TCRδ−/− versus wildtype mice. Neutralization of IL-17A during ozone exposure in wildtype mice mimicked the effects of γδ T cell deficiency. TNFR2 deficiency and etanercept, a TNFα antagonist, also reduced ozone-induced increases in Il17a mRNA, IL-17A+ CD45+ cells and BAL G-CSF as well as BAL neutrophils. TNFR2 deficient mice also had decreased ozone-induced increases in Ccl20, a chemoattractant for IL-17A+ γδ T cells. Il17a mRNA and IL-17A+ γδ T cells were also lower in obese Cpefat versus lean WT mice exposed to subacute ozone, consistent with the reduced neutrophil recruitment observed in the obese mice. Taken together, our data indicate that pulmonary inflammation induced by subacute ozone requires γδ T cells and TNFα-dependent recruitment of IL-17A+ γδ T cells to the lung.en
dc.language.isoen_USen
dc.publisherPublic Library of Scienceen
dc.relation.isversionofdoi:10.1371/journal.pone.0097707en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4019643/pdf/en
dash.licenseLAAen_US
dc.subjectBiology and Life Sciencesen
dc.subjectImmunologyen
dc.subjectImmune Systemen
dc.subjectInnate Immune Systemen
dc.subjectImmunityen
dc.subjectPulmonary Immunologyen
dc.subjectNutritionen
dc.subjectPhysiologyen
dc.subjectPhysiological Parametersen
dc.subjectBody Weighten
dc.subjectObesityen
dc.subjectMedicine and Health Sciencesen
dc.subjectPulmonologyen
dc.subjectAsthmaen
dc.subjectEnvironmental and Occupational Lung Diseasesen
dc.subjectImmunologic Techniquesen
dc.subjectImmunoassaysen
dc.subjectImmunofluorescenceen
dc.subjectModel Organismsen
dc.subjectAnimal Modelsen
dc.subjectMouse Modelsen
dc.titleγδ T Cells Are Required for Pulmonary IL-17A Expression after Ozone Exposure in Mice: Role of TNFαen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalPLoS ONEen
dash.depositing.authorMathews, Joel A.en_US
dc.date.available2014-07-07T18:13:23Z
dc.identifier.doi10.1371/journal.pone.0097707*
dash.contributor.affiliatedBrand, Jeffrey
dash.contributor.affiliatedMathews, Joel A.
dash.contributor.affiliatedKasahara, David
dash.contributor.affiliatedShore, Stephanie


Files in this item

Thumbnail

This item appears in the following Collection(s)

Show simple item record