Source:http://linkedlifedata.com/resource/pubmed/id/17182568
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
1
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| pubmed:dateCreated |
2006-12-21
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| pubmed:abstractText |
A functional immune system not only requires rapid expansion of antigenic specific T cells, but also requires efficient deletion of clonally expanded T cells to avoid accumulation of T cells. Fas/Fas ligand (FasL)-mediated apoptosis plays a critical role in the deletion of activated peripheral T cells, which is clearly demonstrated by superantigen-induced expansion and subsequent deletion of T cells. In this study, we show that in the absence of protein kinase C-theta (PKC-theta), superantigen (staphylococcal enterotoxin B)-induced deletion of Vbeta8(+) CD4(+) T cells was defective in PKC-theta(-/-) mice. In response to staphylococcal enterotoxin B challenge, up-regulation of FasL, but not Fas, was significantly reduced in PKC-theta(-/-) mice. PKC-theta is thus required for maximum up-regulation of FasL in vivo. We further show that stimulation of FasL expression depends on PKC-theta-mediated activation of NF-AT pathway. In addition, PKC-theta(-/-) T cells displayed resistance to Fas-mediated apoptosis as well as activation-induced cell death (AICD). In the absence of PKC-theta, Fas-induced activation of apoptotic molecules such as caspase-8, caspase-3, and Bid was not efficient. However, AICD as well as Fas-mediated apoptosis of PKC-theta(-/-) T cells were restored in the presence of high concentration of IL-2, a critical factor required for potentiating T cells for AICD. PKC-theta is thus required for promoting FasL expression and for potentiating Fas-mediated apoptosis.
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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/BH3 Interacting Domain Death...,
http://linkedlifedata.com/resource/pubmed/chemical/Bid protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 8,
http://linkedlifedata.com/resource/pubmed/chemical/Enterotoxins,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fasl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Isoenzymes,
http://linkedlifedata.com/resource/pubmed/chemical/NFATC Transcription Factors,
http://linkedlifedata.com/resource/pubmed/chemical/Prkcq protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Protein Kinase C,
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 |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:day |
1
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| pubmed:volume |
178
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
312-9
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| pubmed:dateRevised |
2007-11-15
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| pubmed:meshHeading |
pubmed-meshheading:17182568-Animals,
pubmed-meshheading:17182568-Apoptosis,
pubmed-meshheading:17182568-BH3 Interacting Domain Death Agonist Protein,
pubmed-meshheading:17182568-Caspase 3,
pubmed-meshheading:17182568-Caspase 8,
pubmed-meshheading:17182568-Cells, Cultured,
pubmed-meshheading:17182568-Enterotoxins,
pubmed-meshheading:17182568-Fas Ligand Protein,
pubmed-meshheading:17182568-Gene Deletion,
pubmed-meshheading:17182568-Humans,
pubmed-meshheading:17182568-Isoenzymes,
pubmed-meshheading:17182568-Mice,
pubmed-meshheading:17182568-Mice, Mutant Strains,
pubmed-meshheading:17182568-NFATC Transcription Factors,
pubmed-meshheading:17182568-Protein Kinase C,
pubmed-meshheading:17182568-Signal Transduction,
pubmed-meshheading:17182568-T-Lymphocytes,
pubmed-meshheading:17182568-Up-Regulation
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| pubmed:year |
2007
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| pubmed:articleTitle |
The critical role of protein kinase C-theta in Fas/Fas ligand-mediated apoptosis.
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| pubmed:affiliation |
Department of Microbiology and Immunology, School of Medicine, University of Illinois, Chicago, IL 60612, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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