pubmed-article:9317135 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9317135 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
pubmed-article:9317135 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:9317135 | lifeskim:mentions | umls-concept:C0597357 | lld:lifeskim |
pubmed-article:9317135 | lifeskim:mentions | umls-concept:C0021755 | lld:lifeskim |
pubmed-article:9317135 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
pubmed-article:9317135 | lifeskim:mentions | umls-concept:C1880022 | lld:lifeskim |
pubmed-article:9317135 | pubmed:issue | 7 | lld:pubmed |
pubmed-article:9317135 | pubmed:dateCreated | 1997-10-21 | lld:pubmed |
pubmed-article:9317135 | pubmed:abstractText | IL-1 alpha and IL-1 beta bind to receptors termed the type I and type II IL-1 receptors. The type I IL-1 receptor is responsible for specific signaling, while the type II IL-1 receptor functions as a nonsignaling decoy receptor. To determine the effect of a defect in IL-1-mediated signaling, mice have been produced with a genetically disrupted type I IL-1 receptor gene. Mice lacking type I IL-1 receptors are of normal vigor and exhibit no overt phenotype. B cells from type I IL-1R-/- mice activated in vitro with anti-IgM do not proliferate in response to IL-1, but do so in response to IL-4. Injection of murine IL-1 alpha does not induce detectable serum IL-6 levels in type I IL-1R-/- mice, but equivalent levels are produced in response to LPS. Type I IL-1R-/- mice have normal serum Ig levels and generate equivalent primary and secondary Ab responses as wild-type mice. In response to LPS, acute phase protein mRNA induction are equivalent in type I IL-1R-/- and wild-type mice. Type I IL-1R-/- mice do not differ from control mice in susceptibility to either a lethal challenge with D-galactosamine plus LPS or high dose LPS. Interestingly, ICE-/-/type I IL-1R-/- double mutant mice are resistant to high dose LPS. Type I IL-1R-/- mice backcrossed to the C57BL/6 background were as equally resistant as wild-type mice to Listeria monocytogenes. | lld:pubmed |
pubmed-article:9317135 | pubmed:language | eng | lld:pubmed |
pubmed-article:9317135 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9317135 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:9317135 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9317135 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9317135 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9317135 | pubmed:month | Oct | lld:pubmed |
pubmed-article:9317135 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:9317135 | pubmed:author | pubmed-author:SmithJ LJL | lld:pubmed |
pubmed-article:9317135 | pubmed:author | pubmed-author:WillieC DCD | lld:pubmed |
pubmed-article:9317135 | pubmed:author | pubmed-author:LivingstonD... | lld:pubmed |
pubmed-article:9317135 | pubmed:author | pubmed-author:PeschonJ JJJ | lld:pubmed |
pubmed-article:9317135 | pubmed:author | pubmed-author:MorrisseyP... | lld:pubmed |
pubmed-article:9317135 | pubmed:author | pubmed-author:CharrierKK | lld:pubmed |
pubmed-article:9317135 | pubmed:author | pubmed-author:MaliszewskiCC | lld:pubmed |
pubmed-article:9317135 | pubmed:author | pubmed-author:GlaccumM BMB | lld:pubmed |
pubmed-article:9317135 | pubmed:author | pubmed-author:StockingK LKL | lld:pubmed |
pubmed-article:9317135 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9317135 | pubmed:day | 1 | lld:pubmed |
pubmed-article:9317135 | pubmed:volume | 159 | lld:pubmed |
pubmed-article:9317135 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9317135 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9317135 | pubmed:pagination | 3364-71 | lld:pubmed |
pubmed-article:9317135 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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pubmed-article:9317135 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9317135 | pubmed:articleTitle | Phenotypic and functional characterization of mice that lack the type I receptor for IL-1. | lld:pubmed |
pubmed-article:9317135 | pubmed:affiliation | Immunex Corporation, Seattle, WA 98101, USA. | lld:pubmed |
pubmed-article:9317135 | pubmed:publicationType | Journal Article | lld:pubmed |
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