Source:http://linkedlifedata.com/resource/pubmed/id/12077269
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2002-6-21
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| pubmed:abstractText |
Mice lacking the gene for the IL-1R antagonist (IL-1ra) show abnormal development and homeostasis as well as altered responses to infectious and inflammatory stimuli. A reduction in the level of IL-1 signaling, either by deletion of the receptor or increased expression of IL-1ra, does not affect development or homeostasis, but does alter immune responses. In this study we use genetic epistasis to investigate the interdependence of selected genes in the IL-1 family in the regulation of these developmental and immunological processes. Deletion of the gene encoding the type I IL-1R (IL-1RI) is epistatic to deletion of the IL-1ra gene. Therefore, all functions of IL-1ra depend upon the presence of a functional receptor; there is no other target. Similarly, overexpression of the mRNA encoding the secreted form of IL-1ra is epistatic to deletion of the receptor antagonist, leaving the role of the intracellular splice variants of IL-1ra unknown. The abnormal development of IL-1ra-deficient mice is probably due to chronic overstimulation of the proinflammatory pathway via IL-1, but a clear single pathological defect is not apparent. These results support the model that the only essential function of IL-1ra in both health and disease is competitive inhibition of the IL-1RI.
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| pubmed:grant | |
| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Il1rn protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin 1 Receptor Antagonist...,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Interleukin-1,
http://linkedlifedata.com/resource/pubmed/chemical/Sialoglycoproteins
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| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
169
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
393-8
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| pubmed:dateRevised |
2010-11-18
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| pubmed:meshHeading |
pubmed-meshheading:12077269-Animals,
pubmed-meshheading:12077269-Animals, Newborn,
pubmed-meshheading:12077269-Crosses, Genetic,
pubmed-meshheading:12077269-Cytokines,
pubmed-meshheading:12077269-Epistasis, Genetic,
pubmed-meshheading:12077269-Female,
pubmed-meshheading:12077269-Growth Disorders,
pubmed-meshheading:12077269-Homeostasis,
pubmed-meshheading:12077269-Inflammation,
pubmed-meshheading:12077269-Interleukin 1 Receptor Antagonist Protein,
pubmed-meshheading:12077269-Interleukin-1,
pubmed-meshheading:12077269-Listeriosis,
pubmed-meshheading:12077269-Mice,
pubmed-meshheading:12077269-Mice, Inbred C57BL,
pubmed-meshheading:12077269-Mice, Knockout,
pubmed-meshheading:12077269-Mice, Transgenic,
pubmed-meshheading:12077269-Receptors, Interleukin-1,
pubmed-meshheading:12077269-Shock, Septic,
pubmed-meshheading:12077269-Sialoglycoproteins,
pubmed-meshheading:12077269-Survival Analysis
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| pubmed:year |
2002
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| pubmed:articleTitle |
The epistatic interrelationships of IL-1, IL-1 receptor antagonist, and the type I IL-1 receptor.
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| pubmed:affiliation |
Department of Biochemistry and Molecular Biophysics, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
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| pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, U.S. Gov't, P.H.S.
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