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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2003-12-22
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pubmed:abstractText |
The activation of STAT1 and STAT3 in response to SEB was analyzed in spleen of Balb/c mice. The intraperitoneal injection of the superantigen SEB activated STAT1 and STAT3 in spleen. Activated STAT1 almost completely disappeared in 24 h even though activated STAT3 was present for more than 48 h after SEB injection. Cyclosporine A was able to block the initial STAT1 activation, but STAT3 activation was only partially affected. SEB also increased the mRNA levels for STAT1, STAT3 and SOCS1. When a second injection with SEB was given 72 h after the first stimulus, STAT1 activation was much lower than that observed after the first stimulation with SEB and no increase in the STAT1 mRNA level was observed. Nevertheless, after this second injection, STAT3 was again activated without any significant interference from the first stimulus and the STAT3 and SOCS1 mRNA levels again increased. These data indicate that a first stimulation with superantigen re-programs cells so that they respond to a second stimulation in a different way. Understanding the mechanisms implicated in this re-programming is basic for designing therapeutic strategies in processes such as septic shock.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Carrier Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Enterotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Repressor Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/STAT1 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/STAT3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Socs1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Stat1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Stat3 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Superantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Suppressor of Cytokine Signaling...,
http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/enterotoxin B, staphylococcal
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1043-4666
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
7
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pubmed:volume |
25
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1-10
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:14687580-Animals,
pubmed-meshheading:14687580-Carrier Proteins,
pubmed-meshheading:14687580-Cyclosporine,
pubmed-meshheading:14687580-Cytokines,
pubmed-meshheading:14687580-DNA-Binding Proteins,
pubmed-meshheading:14687580-Dimerization,
pubmed-meshheading:14687580-Enterotoxins,
pubmed-meshheading:14687580-Female,
pubmed-meshheading:14687580-Kinetics,
pubmed-meshheading:14687580-Mice,
pubmed-meshheading:14687580-Mice, Inbred BALB C,
pubmed-meshheading:14687580-RNA, Messenger,
pubmed-meshheading:14687580-Repressor Proteins,
pubmed-meshheading:14687580-STAT1 Transcription Factor,
pubmed-meshheading:14687580-STAT3 Transcription Factor,
pubmed-meshheading:14687580-Spleen,
pubmed-meshheading:14687580-Superantigens,
pubmed-meshheading:14687580-Suppressor of Cytokine Signaling Proteins,
pubmed-meshheading:14687580-Trans-Activators,
pubmed-meshheading:14687580-Transcription Factors
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pubmed:year |
2004
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pubmed:articleTitle |
Implication of STAT1 and STAT3 transcription factors in the response to superantigens.
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pubmed:affiliation |
Department of Immunology, Hospital de Sant Pau, Universitat Autonoma de Barcelona, Avda Sant Antoni Maria Claret 167, Barcelona 08025, Spain.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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