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rdf:type |
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lifeskim:mentions |
umls-concept:C0007587,
umls-concept:C0021745,
umls-concept:C0070410,
umls-concept:C0205227,
umls-concept:C0312740,
umls-concept:C0332291,
umls-concept:C1333877,
umls-concept:C1533691,
umls-concept:C1539477,
umls-concept:C1546857,
umls-concept:C1704259,
umls-concept:C1705987
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pubmed:issue |
9
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pubmed:dateCreated |
2002-9-3
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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.
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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/Antibodies, Monoclonal,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/Concanavalin A,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fasl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Granzymes,
http://linkedlifedata.com/resource/pubmed/chemical/Gzmb protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Perforin,
http://linkedlifedata.com/resource/pubmed/chemical/Pore Forming Cytotoxic Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Serine Endopeptidases,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0014-2980
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
32
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2490-9
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12207333-Animals,
pubmed-meshheading:12207333-Antibodies, Monoclonal,
pubmed-meshheading:12207333-Antigens,
pubmed-meshheading:12207333-Antigens, CD3,
pubmed-meshheading:12207333-Antigens, CD95,
pubmed-meshheading:12207333-Antigens, Viral,
pubmed-meshheading:12207333-Apoptosis,
pubmed-meshheading:12207333-Concanavalin A,
pubmed-meshheading:12207333-Exocytosis,
pubmed-meshheading:12207333-Fas Ligand Protein,
pubmed-meshheading:12207333-Granzymes,
pubmed-meshheading:12207333-Interferon-gamma,
pubmed-meshheading:12207333-Lymphocyte Activation,
pubmed-meshheading:12207333-Lymphocytic Choriomeningitis,
pubmed-meshheading:12207333-Lymphocytic choriomeningitis virus,
pubmed-meshheading:12207333-Male,
pubmed-meshheading:12207333-Membrane Glycoproteins,
pubmed-meshheading:12207333-Mice,
pubmed-meshheading:12207333-Mice, Inbred C3H,
pubmed-meshheading:12207333-Mice, Inbred C57BL,
pubmed-meshheading:12207333-Perforin,
pubmed-meshheading:12207333-Pore Forming Cytotoxic Proteins,
pubmed-meshheading:12207333-Serine Endopeptidases,
pubmed-meshheading:12207333-T-Lymphocyte Subsets,
pubmed-meshheading:12207333-Tumor Necrosis Factor-alpha
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pubmed:year |
2002
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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.
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pubmed:affiliation |
Max-Planck-Institut für Immunbiologie, Freiburg, Germany.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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