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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
10
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pubmed:dateCreated |
1995-7-5
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pubmed:abstractText |
Administration of monoclonal antibodies to CD3 triggers acute and massive release of several cytokines, including tumor necrosis factor alpha (TNF-alpha), essentially T cell-derived. This cytokine release is responsible for the spontaneously reversible acute clinical syndrome observed in most OKT3-treated patients. We found that the first OKT3 injection in human renal allograft recipients led to the release in significant amounts of soluble TNF receptors (TNF-sR55 and TNF-sR75) that are considered main natural inhibitors of TNF bioactivity. As for OKT3-induced TNF-alpha, peak TNF-sR levels were observed 1 hr postinjection, and this release was limited to the first monoclonal antibody injection. A distinct regulation of OKT3-mediated release of TNF-sR75 and TNF-sR55 was observed, since (1) in clear contrast with OKT3-mediated TNF-sR75 induction, TNF-sR55 release was completely blocked by a high dose of corticosteroids prior to OKT3 injection and (2) secretion of TNF-sR75 but not TNF-sR55 correlated with immunoreactive TNF-alpha release. In hemodialyzed patients prior to transplantation and OKT3 treatment, a condition characterized by chronic TNF-alpha release, TNF-sR efficiently block TNF bioactivity. In contrast, the system is overwhelmed by the massive acute TNF-alpha release that follows the first OKT3 injection: in such a condition TNF-sR looses its capacity to counteract TNF bioactivity.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adrenal Cortex Hormones,
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antilymphocyte Serum,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
May
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pubmed:issn |
0041-1337
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pubmed:author | |
pubmed:issnType |
Print
|
pubmed:day |
27
|
pubmed:volume |
59
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pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
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pubmed:pagination |
1470-5
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:7770936-Adrenal Cortex Hormones,
pubmed-meshheading:7770936-Antibodies, Monoclonal,
pubmed-meshheading:7770936-Antilymphocyte Serum,
pubmed-meshheading:7770936-Biological Availability,
pubmed-meshheading:7770936-Enzyme-Linked Immunosorbent Assay,
pubmed-meshheading:7770936-Graft Rejection,
pubmed-meshheading:7770936-Humans,
pubmed-meshheading:7770936-Kidney Transplantation,
pubmed-meshheading:7770936-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:7770936-Solubility,
pubmed-meshheading:7770936-Tumor Necrosis Factor-alpha
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pubmed:year |
1995
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pubmed:articleTitle |
In vivo soluble tumor necrosis factor receptor release in OKT3-treated patients. Differential regulation of TNF-sR55 and TNF-sR75.
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pubmed:affiliation |
U 25 INSERM, Association, Claude Bernard, Hôpital Necker, Paris, France.
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pubmed:publicationType |
Journal Article,
Clinical Trial,
Research Support, Non-U.S. Gov't
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