Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
2003-9-8
pubmed:abstractText
The Vgamma4(+) pulmonary subset of gammadelta T cells regulates innate airway responsiveness in the absence of alphabeta T cells. We now have examined the same subset in a model of allergic airway disease, OVA-sensitized and challenged mice that exhibit Th2 responses, pulmonary inflammation, and airway hyperreactivity (AHR). In sensitized mice, Vgamma4(+) cells preferentially increased in number following airway challenge. Depletion of Vgamma4(+) cells before the challenge substantially increased AHR in these mice, but had no effect on airway responsiveness in normal, nonchallenged mice. Depletion of Vgamma1(+) cells had no effect on AHR, and depletion of all TCR-delta(+) cells was no more effective than depletion of Vgamma4(+) cells alone. Adoptively transferred pulmonary lymphocytes containing Vgamma4(+) cells inhibited AHR, but lost this ability when Vgamma4(+) cells were depleted, indicating that these cells actively suppress AHR. Eosinophilic infiltration of the lung and airways, or goblet cell hyperplasia, was not affected by depletion of Vgamma4(+) cells, although cytokine-producing alphabeta T cells in the lung increased. These findings establish Vgamma4(+) gammadelta T cells as negative regulators of AHR and show that their regulatory effect bypasses much of the allergic inflammatory response coincident with AHR.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
171
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3170-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12960345-Adoptive Transfer, pubmed-meshheading:12960345-Animals, pubmed-meshheading:12960345-Bronchial Hyperreactivity, pubmed-meshheading:12960345-Cytokines, pubmed-meshheading:12960345-Female, pubmed-meshheading:12960345-Goblet Cells, pubmed-meshheading:12960345-Hyperplasia, pubmed-meshheading:12960345-Immunization, pubmed-meshheading:12960345-Injections, Intraperitoneal, pubmed-meshheading:12960345-Lymphocyte Count, pubmed-meshheading:12960345-Lymphocyte Depletion, pubmed-meshheading:12960345-Methacholine Chloride, pubmed-meshheading:12960345-Mice, pubmed-meshheading:12960345-Mice, Inbred BALB C, pubmed-meshheading:12960345-Mice, Inbred C57BL, pubmed-meshheading:12960345-Mice, Knockout, pubmed-meshheading:12960345-Ovalbumin, pubmed-meshheading:12960345-Pulmonary Alveoli, pubmed-meshheading:12960345-Pulmonary Eosinophilia, pubmed-meshheading:12960345-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:12960345-Receptors, Antigen, T-Cell, gamma-delta, pubmed-meshheading:12960345-T-Lymphocyte Subsets, pubmed-meshheading:12960345-Up-Regulation
pubmed:year
2003
pubmed:articleTitle
V gamma 4+ gamma delta T cells regulate airway hyperreactivity to methacholine in ovalbumin-sensitized and challenged mice.
pubmed:affiliation
Department of Immunology, National Jewish Medical and Research Center, Denver, CO 80206, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.