pubmed-article:11689551 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11689551 | lifeskim:mentions | umls-concept:C0019704 | lld:lifeskim |
pubmed-article:11689551 | lifeskim:mentions | umls-concept:C0021311 | lld:lifeskim |
pubmed-article:11689551 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:11689551 | lifeskim:mentions | umls-concept:C0007587 | lld:lifeskim |
pubmed-article:11689551 | lifeskim:mentions | umls-concept:C0596952 | lld:lifeskim |
pubmed-article:11689551 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
pubmed-article:11689551 | lifeskim:mentions | umls-concept:C1522538 | lld:lifeskim |
pubmed-article:11689551 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:11689551 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
pubmed-article:11689551 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:11689551 | pubmed:dateCreated | 2002-1-7 | lld:pubmed |
pubmed-article:11689551 | pubmed:abstractText | We have explored in vitro the mechanism by which human immunodeficiency virus, type 1 (HIV-1) induces cell death of primary CD4+ T cells in conditions of productive infection. Although HIV-1 infection primed phytohemagglutinin-activated CD4+ T cells for death induced by anti-CD95 antibody, T cell death was not prevented by a CD95-Fc decoy receptor, nor by decoy receptors of other members of the TNFR family (TNFR1/R2, TRAILR1/R2/OPG, TRAMP) or by various blocking antibodies, suggesting that triggering of death receptors by their cognate ligands is not involved in HIV-induced CD4 T cell death. HIV-1 induced CD4 T cell shrinkage, cell surface exposure of phosphatidylserine, loss of mitochondrial membrane potential (Deltapsim), and mitochondrial release of cytochrome c and apoptosis-inducing factor. A typical apoptotic phenotype (nuclear chromatin condensation and fragmentation) only occurred in around half of the dying cells. Treatment with benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone, a broad spectrum caspase inhibitor, prevented nuclear chromatin condensation and fragmentation in HIV-infected CD4+ T cells and in a cell-free system (in which nuclei were incubated with cytoplasmic extracts from the HIV-infected CD4+ T cells). Nevertheless, benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone did not prevent mitochondrial membrane potential loss and cell death, suggesting that caspases are dispensable for HIV-mediated cell death. Our findings suggest a major role of the mitochondria in the process of CD4 T cell death induced by HIV, in which targeting of Bax to the mitochondria may be involved. | lld:pubmed |
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pubmed-article:11689551 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11689551 | pubmed:language | eng | lld:pubmed |
pubmed-article:11689551 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11689551 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11689551 | pubmed:month | Jan | lld:pubmed |
pubmed-article:11689551 | pubmed:issn | 0021-9258 | lld:pubmed |
pubmed-article:11689551 | pubmed:author | pubmed-author:PetitFrédéric... | lld:pubmed |
pubmed-article:11689551 | pubmed:author | pubmed-author:ArnoultDamien... | lld:pubmed |
pubmed-article:11689551 | pubmed:author | pubmed-author:LelièvreJean-... | lld:pubmed |
pubmed-article:11689551 | pubmed:author | pubmed-author:Moutouh-de... | lld:pubmed |
pubmed-article:11689551 | pubmed:author | pubmed-author:HanceAllan... | lld:pubmed |
pubmed-article:11689551 | pubmed:author | pubmed-author:SchneiderPasc... | lld:pubmed |
pubmed-article:11689551 | pubmed:author | pubmed-author:CorbeilJacque... | lld:pubmed |
pubmed-article:11689551 | pubmed:author | pubmed-author:AmeisenJean... | lld:pubmed |
pubmed-article:11689551 | pubmed:author | pubmed-author:EstaquierJérô... | lld:pubmed |
pubmed-article:11689551 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:11689551 | pubmed:day | 11 | lld:pubmed |
pubmed-article:11689551 | pubmed:volume | 277 | lld:pubmed |
pubmed-article:11689551 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11689551 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11689551 | pubmed:pagination | 1477-87 | lld:pubmed |
pubmed-article:11689551 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:11689551 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:11689551 | pubmed:articleTitle | Productive HIV-1 infection of primary CD4+ T cells induces mitochondrial membrane permeabilization leading to a caspase-independent cell death. | lld:pubmed |
pubmed-article:11689551 | pubmed:affiliation | INSERM EMI-U 9922, CHU Bichat, Université Paris 7, 16 rue Henri Huchard, 75018 Paris, France. | lld:pubmed |
pubmed-article:11689551 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11689551 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:11689551 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
pubmed-article:11689551 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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