| pubmed-article:12207333 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C0312740 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C0021745 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C0070410 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C1333877 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C1539477 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C1533691 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C1546857 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
| pubmed-article:12207333 | lifeskim:mentions | umls-concept:C0332291 | lld:lifeskim |
| pubmed-article:12207333 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:12207333 | pubmed:dateCreated | 2002-9-3 | lld:pubmed |
| pubmed-article:12207333 | pubmed:abstractText | Activation of resting T cells usually leads to their proliferation and differentiation into effector cells and a subsequent decline following elimination of the antigen. A situation of excessive antigen density may result in T cell receptor (TCR)-induced deletion of T effector cells, a process termed antigen-induced cell death (AgICD). Previous studies indicate that AgICD of cytotoxic T cells may be induced by either of the two key cytotoxic processes, granule exocytosis, including perforin and granzymes, or the Fas ligand (FasL)/Fas pathway. By using in vitro-polyclonally activated or ex vivo-derived virus-induced T cell populations from mice with mutations or targeted gene defects in one or more components of the two key cytolytic pathways we now show that TCR-induced apoptosis is only impaired in the absence of FasL and/or Fas, but not in the absence of perforin and/or granzymes. Furthermore, antibody-blockage of FasL alone is sufficient to inhibit early T cell death. Inhibition of both, FasL and tumor necrosis factor (TNF-alpha) is required to abrogate late apoptosis by AgICD. The fact that antibodies to IFN-gamma also inhibit AgICD suggests that the perforin plus granzyme-independent and FaSL and/or TNF-alpha facilitated process of AgICD of T effector cells is tightly regulated by endogenous IFN-gamma. | lld:pubmed |
| pubmed-article:12207333 | pubmed:language | eng | lld:pubmed |
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| pubmed-article:12207333 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:12207333 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12207333 | pubmed:month | Sep | lld:pubmed |
| pubmed-article:12207333 | pubmed:issn | 0014-2980 | lld:pubmed |
| pubmed-article:12207333 | pubmed:author | pubmed-author:KörnerHeinric... | lld:pubmed |
| pubmed-article:12207333 | pubmed:author | pubmed-author:SimonMarkus... | lld:pubmed |
| pubmed-article:12207333 | pubmed:author | pubmed-author:BalkowSandraS | lld:pubmed |
| pubmed-article:12207333 | pubmed:author | pubmed-author:SobekVeraV | lld:pubmed |
| pubmed-article:12207333 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:12207333 | pubmed:volume | 32 | lld:pubmed |
| pubmed-article:12207333 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12207333 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12207333 | pubmed:pagination | 2490-9 | lld:pubmed |
| pubmed-article:12207333 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:12207333 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12207333 | pubmed:articleTitle | Antigen-induced cell death of T effector cells in vitro proceeds via the Fas pathway, requires endogenous interferon-gamma and is independent of perforin and granzymes. | lld:pubmed |
| pubmed-article:12207333 | pubmed:affiliation | Max-Planck-Institut für Immunbiologie, Freiburg, Germany. | lld:pubmed |
| pubmed-article:12207333 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12207333 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:12207333 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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