Source:http://linkedlifedata.com/resource/pubmed/id/18441236
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2008-8-7
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pubmed:abstractText |
T-cell depletion associated with HIV infection or cytoreductive therapies triggers potential T-cell regenerative mechanisms such as peripheral T-lymphocyte expansion to weak antigenic stimuli and the increased availability of interleukin-7 (IL-7), a cytokine with potent antiapoptotic and proliferative activities. Deleterious mechanisms also associated with lymphopenia, such as increased Fas expression and apoptosis of T cell, however, may result in opposing effects. In this study, we show that Fas molecules, primarily associated with T-cell depletion in lymphopenic settings, may also contribute to compensatory T-cell expansion through transmitting costimulatory signals to suboptimally activated T cells. Proliferation of T lymphocytes in response to concomitant Fas and T-cell receptor (TCR) triggering was shown to be increased in HIV-infected individuals compared with noninfected controls. As IL-7 levels are often elevated in lymphopenic individuals in association with increased Fas expression, we analyzed whether IL-7 would influence Fas-mediated proliferative signals in T cells. We show that IL-7 is able to increase the efficacy of Fas to induce proliferation of suboptimally activated T cells. Thus, high IL-7 levels associated with lymphopenic conditions may simultaneously induce sensitivity to Fas-mediated apoptosis in nonactivated T cells and increase Fas-induced costimulatory signals in T cells recognizing low-affinity antigens.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1528-0020
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
112
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1195-204
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pubmed:meshHeading |
pubmed-meshheading:18441236-Antigen Presentation,
pubmed-meshheading:18441236-Antigens, CD95,
pubmed-meshheading:18441236-Apoptosis,
pubmed-meshheading:18441236-Case-Control Studies,
pubmed-meshheading:18441236-Cell Proliferation,
pubmed-meshheading:18441236-Female,
pubmed-meshheading:18441236-HIV Infections,
pubmed-meshheading:18441236-Humans,
pubmed-meshheading:18441236-Interleukin-7,
pubmed-meshheading:18441236-Lymphopenia,
pubmed-meshheading:18441236-Male,
pubmed-meshheading:18441236-T-Lymphocytes
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pubmed:year |
2008
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pubmed:articleTitle |
Priming of T cells to Fas-mediated proliferative signals by interleukin-7.
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pubmed:affiliation |
Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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