|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0021745,
umls-concept:C0021764,
umls-concept:C0178719,
umls-concept:C0205314,
umls-concept:C0218229,
umls-concept:C0300926,
umls-concept:C0332120,
umls-concept:C0439831,
umls-concept:C0441712,
umls-concept:C0679622,
umls-concept:C0851285,
umls-concept:C0871261,
umls-concept:C1698986,
umls-concept:C1704632,
umls-concept:C1706817,
umls-concept:C2003941,
umls-concept:C2911692
|
|
pubmed:issue |
12
|
|
pubmed:dateCreated |
2002-3-18
|
|
pubmed:abstractText |
Interleukin (IL)-13 mediates its activities via a complex receptor system. Interleukin-13 receptor alpha-1 chain (IL-13Ralpha1) binds IL-13 with low affinity, but does not signal. However, when IL-13Ralpha1 combines with IL-4 receptor alpha (IL-4Ralpha), a signaling high affinity receptor complex for IL-13 is generated. In contrast, IL-13Ralpha2 alone binds IL-13 with high affinity, but does not signal and has been postulated to be a decoy receptor. Herein, we investigated the cellular localization of IL-13Ralpha2 and the regulation of its expression by confocal microscopy and flow cytometry in primary and cultured cells. Our results demonstrate that IL-13Ralpha2 is largely an intracellular molecule, which is rapidly mobilized from intracellular stores following treatment with interferon (IFN)-gamma. Up-regulation of IL-13Ralpha2 surface expression in response to IFN-gamma was rapid, did not require protein synthesis, and resulted in diminished IL-13 signaling. These results provide the first evidence that the IL-13Ralpha2 is predominantly an intracellular molecule and demonstrate a novel mechanism by which IFN-gamma can regulate IL-13 responses.
|
|
pubmed:grant |
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
IM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Mar
|
|
pubmed:issn |
0021-9258
|
|
pubmed:author |
|
|
pubmed:issnType |
Print
|
|
pubmed:day |
22
|
|
pubmed:volume |
277
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
10387-93
|
|
pubmed:dateRevised |
2008-11-21
|
|
pubmed:meshHeading |
pubmed-meshheading:11786536-Amino Acid Motifs,
pubmed-meshheading:11786536-Cells, Cultured,
pubmed-meshheading:11786536-Dose-Response Relationship, Drug,
pubmed-meshheading:11786536-Flow Cytometry,
pubmed-meshheading:11786536-Gene Expression Regulation,
pubmed-meshheading:11786536-Humans,
pubmed-meshheading:11786536-Interferon-gamma,
pubmed-meshheading:11786536-Interleukin-13,
pubmed-meshheading:11786536-Interleukin-13 Receptor alpha1 Subunit,
pubmed-meshheading:11786536-Interleukin-4,
pubmed-meshheading:11786536-Kinetics,
pubmed-meshheading:11786536-Microscopy, Confocal,
pubmed-meshheading:11786536-Monocytes,
pubmed-meshheading:11786536-Protein Binding,
pubmed-meshheading:11786536-Receptors, Interleukin,
pubmed-meshheading:11786536-Receptors, Interleukin-13,
pubmed-meshheading:11786536-Signal Transduction,
pubmed-meshheading:11786536-Time Factors,
pubmed-meshheading:11786536-U937 Cells,
pubmed-meshheading:11786536-Up-Regulation
|
|
pubmed:year |
2002
|
|
pubmed:articleTitle |
A novel mechanism by which interferon-gamma can regulate interleukin (IL)-13 responses. Evidence for intracellular stores of IL-13 receptor alpha -2 and their rapid mobilization by interferon-gamma.
|
|
pubmed:affiliation |
Division of Allergy and Immunology, Department of Pediatrics, Children's Hospital Medical Center, Cincinnati, Ohio 45229, USA.
|
|
pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|
