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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2006-6-14
pubmed:abstractText
Eosinophilic inflammation in the bronchial mucosa has been recognized as a prominent pathological feature of bronchial asthma. Th2 cells have been implicated in the local infiltration and activation of eosinophils. The migration of eosinophils as well as Th2 cells is controlled by chemokines, suggesting a crucial role of chemokines in the pathogenesis of bronchial asthma. To elucidate the mechanism by which Th2 cells induce eosinophilic inflammation, a Th2-cell-dependent murine model of asthma was employed in this study. Along with the infiltration of eosinophils and antigen-specific Th2 cells, CC chemokine receptor-3-active eotaxin, monocyte chemoattractant protein (MCP)-3 and RANTES, as well as CC chemokine receptor-3-inactive MCP-1 were produced in the lungs of Th2-cell-transferred mice after antigen provocation in vivo. On the other hand, differentiated antigen-specific Th2 cells produced MCP-3 and RANTES but not eotaxin or MCP-1 upon stimulation in vitro. Chemokines synthesized by Th2 cells and other cell types are involved in the development of eosinophilic inflammation in bronchial asthma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1018-2438
pubmed:author
pubmed:copyrightInfo
Copyright 2006 S. Karger AG, Basel.
pubmed:issnType
Print
pubmed:volume
140 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
55-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Th2-cell-mediated chemokine synthesis is involved in allergic airway inflammation in mice.
pubmed:affiliation
Clinical Research Center for Allergy and Rheumatology, National Hospital Organization, Sagamihara National Hospital, Kanagawa, Japan. mori-kkr@umin.ac.jp
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't