Linked Life Data

20501609

Source:http://linkedlifedata.com/resource/pubmed/id/20501609

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2010-5-28
pubmed:abstractText
Adoptive cell transfer of an ovalbumin (OVA)-specific T(h)17-polarized cell population from transgenic DO11.10 mice into BALB/c mice followed by OVA inhalation caused airway hyperresponsiveness (AHR) with severe neutrophilia. The transferred T(h)17 cell population-previously polarized in vitro with IL-6, transforming growth factor-beta and IL-23-contained negligible numbers of IFN-gamma-producing cells; however, during T(h)17-cell-dependent airway inflammation, significant numbers of IFN-gamma-producing cells-including cells producing both IL-17 and IFN-gamma and cells producing only IFN-gamma-were detected in the lung in addition to cells producing only IL-17. Using T(h)17-polarized cell populations derived from IL-17(-/-) or IFN-gamma(-/-) mice, it was demonstrated that IL-17 is essential for inducing neutrophilic airway inflammation and that IFN-gamma is required for the AHR elevation. IFN-gamma appeared to be derived from cells producing both IL-17 and IFN-gamma and/or from cells producing only IFN-gamma, which were converted from the transferred T(h)17-polarized cell population. We also found that mAbs that neutralize IL-12 significantly suppressed the conversion of the T(h)17-polarized cell population toward IFN-gamma producers in the lung; concomitantly, with this decreased conversion, IL-12 neutralization also attenuated the AHR elevation in the lung. IL-12-dependent conversion of the transferred T(h)17-polarized cell population into IFN-gamma producers in the lung thus appeared to be a crucial process for inducing AHR elevation in T(h)17-cell-dependent airway inflammation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1460-2377
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
22
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
503-13
pubmed:meshHeading
pubmed-meshheading:20501609-Adoptive Transfer, pubmed-meshheading:20501609-Animals, pubmed-meshheading:20501609-Antibodies, Blocking, pubmed-meshheading:20501609-Bronchial Hyperreactivity, pubmed-meshheading:20501609-Cell Movement, pubmed-meshheading:20501609-Cells, Cultured, pubmed-meshheading:20501609-Disease Models, Animal, pubmed-meshheading:20501609-Interferon-gamma, pubmed-meshheading:20501609-Interleukin-12, pubmed-meshheading:20501609-Interleukin-17, pubmed-meshheading:20501609-Lung, pubmed-meshheading:20501609-Mice, pubmed-meshheading:20501609-Mice, Inbred BALB C, pubmed-meshheading:20501609-Mice, Knockout, pubmed-meshheading:20501609-Mice, Transgenic, pubmed-meshheading:20501609-Neutrophils, pubmed-meshheading:20501609-Ovalbumin, pubmed-meshheading:20501609-Receptors, Antigen, T-Cell, pubmed-meshheading:20501609-T-Lymphocyte Subsets, pubmed-meshheading:20501609-T-Lymphocytes, Helper-Inducer
pubmed:year
2010
pubmed:articleTitle
A T(h)17-polarized cell population that has infiltrated the lung requires cells that convert to IFN-{gamma} production in order to induce airway hyperresponsiveness.
pubmed:affiliation
Institute for Genetic Medicine, Hokkaido University, Sapporo, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't