Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2010-7-27
pubmed:abstractText
Antagonists of the type 1 cysteinyl leukotriene receptor (CysLT(1)R) are efficacious for bronchoconstriction in humans with bronchial asthma; however, the clinical response to these drugs is heterogeneous. In particular, how CysLT(1)R expression and function are constitutively regulated in vivo is not known. In this study, we show that a seven-transmembrane receptor, GPR17, negatively regulates the CysLT(1)R-mediated inflammatory cell accumulation in the bronchoalveolar lavage fluid and lung, the levels of IgE and specific IgG1 in serum, and Th2/Th17 cytokine expression in the lung after intranasal sensitization and challenge with the house dust mite (extract of Dermatophagoides farinae [Df]) in mice. Sensitization of naive wild-type recipients with Df-pulsed bone marrow-derived dendritic cells of each genotype or sensitization of each genotype with Df-pulsed wild-type bone marrow-derived dendritic cells and Df challenge revealed markedly increased pulmonary inflammatory and serum IgE responses for GPR17-deficient mice as compared with wild-type mice and reduced responses in the genotypes lacking CysLT(1)R. These findings reveal a constitutive negative regulation of CysLT(1)R functions by GPR17 in both the Ag presentation and downstream phases of allergic pulmonary inflammation.
pubmed:grant
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
185
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1846-54
pubmed:dateRevised
2010-9-27
pubmed:meshHeading
pubmed-meshheading:20574000-Allergens, pubmed-meshheading:20574000-Animals, pubmed-meshheading:20574000-Antigen Presentation, pubmed-meshheading:20574000-Cell Movement, pubmed-meshheading:20574000-Dermatophagoides farinae, pubmed-meshheading:20574000-Desensitization, Immunologic, pubmed-meshheading:20574000-Dose-Response Relationship, Immunologic, pubmed-meshheading:20574000-Female, pubmed-meshheading:20574000-Immunoglobulin E, pubmed-meshheading:20574000-Immunoglobulin G, pubmed-meshheading:20574000-Inflammation, pubmed-meshheading:20574000-Interleukin-17, pubmed-meshheading:20574000-Lung, pubmed-meshheading:20574000-Lymph Nodes, pubmed-meshheading:20574000-Male, pubmed-meshheading:20574000-Mice, pubmed-meshheading:20574000-Mice, Inbred C57BL, pubmed-meshheading:20574000-Mice, Knockout, pubmed-meshheading:20574000-Nerve Tissue Proteins, pubmed-meshheading:20574000-Receptors, G-Protein-Coupled, pubmed-meshheading:20574000-Receptors, Leukotriene, pubmed-meshheading:20574000-Respiratory Hypersensitivity, pubmed-meshheading:20574000-Th2 Cells
pubmed:year
2010
pubmed:articleTitle
GPR17 regulates immune pulmonary inflammation induced by house dust mites.
pubmed:affiliation
Department of Medicine, Harvard Medical School and Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, MA 02115, USA. amaekawa@rics.bwh.harvard.edu
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural