Source:http://linkedlifedata.com/resource/pubmed/id/18327975
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rdf:type | |
lifeskim:mentions |
umls-concept:C0007600,
umls-concept:C0019682,
umls-concept:C0019699,
umls-concept:C0033268,
umls-concept:C0039194,
umls-concept:C0162638,
umls-concept:C0205216,
umls-concept:C0332307,
umls-concept:C0812246,
umls-concept:C1456820,
umls-concept:C1521840,
umls-concept:C1522538,
umls-concept:C1533691,
umls-concept:C1627358,
umls-concept:C2349975
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pubmed:issue |
3
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pubmed:dateCreated |
2008-3-31
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pubmed:abstractText |
OX40, a member of the tumor necrosis factor receptor (TNF-R) superfamily, has been shown to play an important role in the survival of antigen-specific CD4(+) T cells. We have previously reported that stimulation of the OX40-expressing and HIV-1 chronically infected T cell line, ACH-2/OX40, with either OX40 ligand (OX40L)-expressing cells or with TNF resulted in the activation of HIV-1 followed by apoptotic cell death. In the present study we found that costimulation via OX40 and TNF-R in OX40-expressing HIV-1-infected T cell lines leads to a marked reduction of HIV-1 production associated with rapid cell death. Since HIV-1-negative OX40(+) T cell lines underwent rapid apoptotic cell death after OX40L and TNF stimulation, it was reasoned that the ACH-2/OX40 cell death was unlikely to be due to HIV-1 infection. Furthermore, we found that the OX40-mediated apoptosis of the CD4(+) T cell line, Molt-4/CCR5-OX40 (M/R5-OX40), required (1) signals mediated via the cytoplasmic tail of OX40, (2) activation of the caspase cascade, including caspase-8 and caspase-3, and (3) induction of endogenous TNF-alpha, but not of TNF-beta, FasL, or TNF-related apoptosis-inducing ligand (TRAIL), suggesting that this apoptosis occurred indirectly via the TNF/TNF-R system. Finally, a fraction of primary activated CD4(+) T cells, expressing high levels of OX40, underwent apoptosis, as revealed by annexin V staining, after cocultivation with OX40L(+) cells. These results suggest a new biological role of the OX40L/OX40 system in controlling the fate of activated CD4(+) T cells and of controlling HIV-1 infection in inflammatory environments.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Annexin A5,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 3,
http://linkedlifedata.com/resource/pubmed/chemical/Caspase 8,
http://linkedlifedata.com/resource/pubmed/chemical/HIV Core Protein p24,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, OX40,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor,
http://linkedlifedata.com/resource/pubmed/chemical/TNFRSF4 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Tumor Necrosis Factor-alpha,
http://linkedlifedata.com/resource/pubmed/chemical/p24 protein, Human...
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0889-2229
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
24
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
423-35
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pubmed:meshHeading |
pubmed-meshheading:18327975-Animals,
pubmed-meshheading:18327975-Annexin A5,
pubmed-meshheading:18327975-Apoptosis,
pubmed-meshheading:18327975-Caspase 3,
pubmed-meshheading:18327975-Caspase 8,
pubmed-meshheading:18327975-Cell Line,
pubmed-meshheading:18327975-Cell Survival,
pubmed-meshheading:18327975-HIV Core Protein p24,
pubmed-meshheading:18327975-HIV-1,
pubmed-meshheading:18327975-Humans,
pubmed-meshheading:18327975-Mice,
pubmed-meshheading:18327975-Receptors, OX40,
pubmed-meshheading:18327975-Receptors, Tumor Necrosis Factor,
pubmed-meshheading:18327975-T-Lymphocytes,
pubmed-meshheading:18327975-Tumor Necrosis Factor-alpha
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pubmed:year |
2008
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pubmed:articleTitle |
Enhancement of OX40-induced apoptosis by TNF coactivation in OX40-expressing T cell lines in vitro leading to decreased targets for HIV type 1 production.
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pubmed:affiliation |
Department of Immunology, Graduate School of Medicine, University of the Ryukyus, Nishihara, Okinawa 903-0215, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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