| pubmed-article:17182568 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17182568 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:17182568 | lifeskim:mentions | umls-concept:C0162638 | lld:lifeskim |
| pubmed-article:17182568 | lifeskim:mentions | umls-concept:C0033640 | lld:lifeskim |
| pubmed-article:17182568 | lifeskim:mentions | umls-concept:C1539477 | lld:lifeskim |
| pubmed-article:17182568 | lifeskim:mentions | umls-concept:C1511545 | lld:lifeskim |
| pubmed-article:17182568 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:17182568 | pubmed:dateCreated | 2006-12-21 | lld:pubmed |
| pubmed-article:17182568 | 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. | lld:pubmed |
| pubmed-article:17182568 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17182568 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17182568 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17182568 | pubmed:citationSubset | AIM | lld:pubmed |
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| pubmed-article:17182568 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17182568 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:17182568 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:17182568 | pubmed:author | pubmed-author:SunZuomingZ | lld:pubmed |
| pubmed-article:17182568 | pubmed:author | pubmed-author:ManicassamySa... | lld:pubmed |
| pubmed-article:17182568 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17182568 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:17182568 | pubmed:volume | 178 | lld:pubmed |
| pubmed-article:17182568 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17182568 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17182568 | pubmed:pagination | 312-9 | lld:pubmed |
| pubmed-article:17182568 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:17182568 | pubmed:year | 2007 | lld:pubmed |
| pubmed-article:17182568 | pubmed:articleTitle | The critical role of protein kinase C-theta in Fas/Fas ligand-mediated apoptosis. | lld:pubmed |
| pubmed-article:17182568 | pubmed:affiliation | Department of Microbiology and Immunology, School of Medicine, University of Illinois, Chicago, IL 60612, USA. | lld:pubmed |
| pubmed-article:17182568 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17182568 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17182568 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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