Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-4-21
pubmed:abstractText
IL-13 is an immunoregulatory cytokine secreted predominantly by activated T(H)2 cells. Over the past several years, it has become evident that IL-13 is a key mediator in the pathogenesis of allergic inflammation. IL-13 shares many functional properties with IL-4, stemming from the fact that they share a common receptor subunit, the alpha subunit of the IL-4 receptor (IL-4Ralpha). Characterization of IL-13-deficient mice, IL-4-deficient mice, and IL-4 receptor alpha-deficient (IL-4Ralpha(-/-)) mice have demonstrated nonredundant roles for IL-13. IL-13 mediates its effects by interacting with a complex receptor system comprised of IL-4Ralpha and two IL-13 binding proteins, IL-13Ralpha1 and IL-13Ralpha2. IL-13 receptors are expressed on human B cells, basophils, eosinophils, mast cells, endothelial cells, fibroblasts, monocytes, macrophages, respiratory epithelial cells, and smooth muscle cells. However, functional IL-13 receptors have not been demonstrated on human or mouse T cells. Thus unlike IL-4, IL-13 does not appear to be important in the initial differentiation of CD4 T cells into T(H)2-type cells but rather appears to be important in the effector phase of allergic inflammation. This is further supported by many in vivo observations, including that administration of IL-13 resulted in allergic inflammation, tissue-specific overexpression of IL-13 in the lungs of transgenic mice resulted in airway inflammation and mucus hypersecretion, IL-13 blockade abolished allergic inflammation independently of IL-4, and IL-13 appears to be more important than IL-4 in mucus hypersecretion. Given the importance of IL-13 as an effector molecule, regulation at the level of its receptors might be an important mechanism of modulating IL-13 responses and thus propagation of the allergic response. Accordingly, IL-13 is an attractive, novel therapeutic target for pharmacologic intervention in allergic disorders. This review will summarize the current understanding of the IL-13 receptors and signaling pathways, emphasizing recent observations.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines, http://linkedlifedata.com/resource/pubmed/chemical/IL13RA1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Il13ra1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-13, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-13 Receptor alpha1..., http://linkedlifedata.com/resource/pubmed/chemical/JAK1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Jak1 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Janus Kinase 1, http://linkedlifedata.com/resource/pubmed/chemical/Protein-Tyrosine Kinases, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-13, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-4, http://linkedlifedata.com/resource/pubmed/chemical/STAT6 Transcription Factor, http://linkedlifedata.com/resource/pubmed/chemical/STAT6 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0091-6749
pubmed:author
pubmed:issnType
Print
pubmed:volume
111
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
677-90; quiz 691
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
IL-13 receptors and signaling pathways: an evolving web.
pubmed:affiliation
Division of Allergy, and Immunology, Department of Pediatrics, Cincinnati Children's Hospital Medical Center, Cincinnati, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review