Linked Life Data

14561170

Source:http://linkedlifedata.com/resource/pubmed/id/14561170

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2003-10-16
pubmed:abstractText
Asthma is characterized by elevated production of IgE, Th2 cytokines, chemokines, mucus hypersecretion, globlet cell metaplasia/hyperplasia, airway obstruction, eosinophilia and enhanced bronchial hyperresponsiveness. These hallmark features of asthma have all been linked to the effector functions of Th2 cytokines (e.g., interleukin-(IL)-4,5,9,10, and 13) in clinical and experimental investigations. This article will detail some of the pathogenic effects regulated by IL-13, IL-5 and the eotaxin subfamily of chemokines to regulate certain aspects of allergic disease. In particular, the potency of IL-13 in inducing enhanced bronchial responsiveness to spasmogenic stimuli and mucus hypersecretion suggests a key role of this molecule in the induction of airways obstruction. Recent studies also indicate that IL-5 and eotaxin, through eosinophils, may regulate Th2 cell function and IL-13 production from this lymphocyte. Therefore, IL-5 and IL-13 signaling systems are not necessarily mutually exclusive effector mechanisms, but may also be integrated through eosinophils to regulate certain aspects of allergic diseases. Blocking IL-13, or pathways that may promote IL-13-associated allergic lung responses (IL-5 and eotaxin) could provide an important strategy to improve the specificity of asthma therapy.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
1568-010X
pubmed:author
pubmed:issnType
Print
pubmed:volume
2
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
169-74
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Regulation of eosinophil migration and Th2 cell function by IL-5 and eotaxin.
pubmed:affiliation
Department of Pediatrics and Adolescent Medicine, University of Freiburg, Mathildenstr. 1, 79106 Freiburg, Germany. mattes@kkl200.ukl.uni-freiburg.de
pubmed:publicationType
Journal Article, Review