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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2009-5-21
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pubmed:abstractText |
We had shown earlier that the concentrations of circulating interleukin-18 (IL-18) are increased significantly in human immunodeficiency virus (HIV)-infected persons compared to HIV-seronegative healthy subjects. In the present study, we investigated the consequences of these elevated levels of IL-18 on natural killer (NK) cells and the immunopathogenesis of AIDS. We show here an inverse correlation between IL-18 concentrations and absolute numbers of various subsets of NK cells in infected persons. Recombinant human IL-18 caused increased death of a human NK cell line, as well as of primary human NK cells in vitro. The IL-18-mediated cell death was dependent upon Fas-FasL interactions and tumor necrosis factor alpha. IL-18 induced the expression of FasL on NK cells, increased the transcription from the human FasL promoter, reduced the expression of Bcl-X(L) in NK cells, and increased their sensitivity to FasL-mediated cell death. These results suggest that increased IL-18 concentrations present in the circulation of HIV-infected persons contribute to the immunopathogenesis of AIDS by altering NK cell homeostasis.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-10395644,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-10644334,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-10807199,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-10807517,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-10903731,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-11061668,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-11244043,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-11315928,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-11403230,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-12438570,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-12850795,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-16020503,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-16203865,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-16239902,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-16542373,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-17032165,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-17073617,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-1708784,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-17336692,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-18388298,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-18388299,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-18836917,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-2492265,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-7477296,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-7500022,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-7516670,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-7689810,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-7908324,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-7908983,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-8093360,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-8892629,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-8912881,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-9028322,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-9378984,
http://linkedlifedata.com/resource/pubmed/commentcorrection/19339355-9632757
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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 |
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1098-5514
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
83
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
5999-6010
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pubmed:dateRevised |
2010-9-23
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pubmed:meshHeading |
pubmed-meshheading:19339355-Acquired Immunodeficiency Syndrome,
pubmed-meshheading:19339355-Antigens, CD95,
pubmed-meshheading:19339355-Cell Death,
pubmed-meshheading:19339355-Cell Line,
pubmed-meshheading:19339355-Fas Ligand Protein,
pubmed-meshheading:19339355-Gene Expression Regulation,
pubmed-meshheading:19339355-HIV-1,
pubmed-meshheading:19339355-Humans,
pubmed-meshheading:19339355-Interleukin-18,
pubmed-meshheading:19339355-Killer Cells, Natural,
pubmed-meshheading:19339355-Promoter Regions, Genetic,
pubmed-meshheading:19339355-Transcription, Genetic,
pubmed-meshheading:19339355-Tumor Necrosis Factor-alpha,
pubmed-meshheading:19339355-bcl-X Protein
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pubmed:year |
2009
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pubmed:articleTitle |
Potential role of interleukin-18 in the immunopathogenesis of AIDS: involvement in fratricidal killing of NK cells.
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pubmed:affiliation |
Department of Microbiology and Immunology, Laboratory of Innate Immunity, CHU-Sainte-Justine Research Center, University of Montreal, Montreal, Quebec, Canada.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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