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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2001-1-26
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pubmed:abstractText |
Activation-induced cell death (AICD) of mature T cells plays an important role in the control of immune homeostasis and peripheral tolerance. TNFRs and Fas have been implicated in the induction of AICD. However, these molecules were shown to be dispensable, at least in some experimental systems, for downsizing of Ag-induced T cell expansions and development of tolerance in vivo. The conditions of T cell activation leading to T cell deletion in a death receptor-independent manner are not well characterized. Here we show that human CTLs die through a death receptor-independent apoptotic program upon triggering with a partially agonistic peptide ligand. This apoptotic process exhibits some features of T cell death due to lymphokine deprivation and is blocked by exogenous IL-2. Our data demonstrate that engagement of TCR by MHC-peptide complexes can trigger diverse apoptotic programs of AICD and that the choice between these programs is determined by the agonistic potency of MHC-peptide ligand.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/BCL2L1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Bcl2l1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclosporine,
http://linkedlifedata.com/resource/pubmed/chemical/Epstein-Barr Virus Nuclear Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/FASLG protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fasl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-A Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/HLA-A11 Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins c-bcl-2,
http://linkedlifedata.com/resource/pubmed/chemical/bcl-X Protein
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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 |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
166
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
989-95
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:11145677-Animals,
pubmed-meshheading:11145677-Antigens, CD95,
pubmed-meshheading:11145677-Apoptosis,
pubmed-meshheading:11145677-Cell Death,
pubmed-meshheading:11145677-Cell Differentiation,
pubmed-meshheading:11145677-Cell Line,
pubmed-meshheading:11145677-Cell Survival,
pubmed-meshheading:11145677-Clone Cells,
pubmed-meshheading:11145677-Cyclosporine,
pubmed-meshheading:11145677-Epstein-Barr Virus Nuclear Antigens,
pubmed-meshheading:11145677-Fas Ligand Protein,
pubmed-meshheading:11145677-HLA-A Antigens,
pubmed-meshheading:11145677-HLA-A11 Antigen,
pubmed-meshheading:11145677-Humans,
pubmed-meshheading:11145677-Interleukin-2,
pubmed-meshheading:11145677-Kinetics,
pubmed-meshheading:11145677-Ligands,
pubmed-meshheading:11145677-Lymphocyte Activation,
pubmed-meshheading:11145677-Membrane Glycoproteins,
pubmed-meshheading:11145677-Mice,
pubmed-meshheading:11145677-Peptide Fragments,
pubmed-meshheading:11145677-Proto-Oncogene Proteins c-bcl-2,
pubmed-meshheading:11145677-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:11145677-Tumor Cells, Cultured,
pubmed-meshheading:11145677-Up-Regulation,
pubmed-meshheading:11145677-bcl-X Protein
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pubmed:year |
2001
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pubmed:articleTitle |
Different programs of activation-induced cell death are triggered in mature activated CTL by immunogenic and partially agonistic peptide ligands.
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pubmed:affiliation |
Microbiology and Tumor Biology Center, Karolinska Institutet, Stockholm, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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