pubmed-article:18441236 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18441236 | lifeskim:mentions | umls-concept:C0021761 | lld:lifeskim |
pubmed-article:18441236 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:18441236 | lifeskim:mentions | umls-concept:C0334094 | lld:lifeskim |
pubmed-article:18441236 | lifeskim:mentions | umls-concept:C1710082 | lld:lifeskim |
pubmed-article:18441236 | pubmed:issue | 4 | lld:pubmed |
pubmed-article:18441236 | pubmed:dateCreated | 2008-8-7 | lld:pubmed |
pubmed-article:18441236 | 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. | lld:pubmed |
pubmed-article:18441236 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18441236 | pubmed:language | eng | lld:pubmed |
pubmed-article:18441236 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18441236 | pubmed:citationSubset | AIM | lld:pubmed |
pubmed-article:18441236 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18441236 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18441236 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18441236 | pubmed:month | Aug | lld:pubmed |
pubmed-article:18441236 | pubmed:issn | 1528-0020 | lld:pubmed |
pubmed-article:18441236 | pubmed:author | pubmed-author:RajnavolgyiEv... | lld:pubmed |
pubmed-article:18441236 | pubmed:author | pubmed-author:RethiBenceB | lld:pubmed |
pubmed-article:18441236 | pubmed:author | pubmed-author:ChiodiFrances... | lld:pubmed |
pubmed-article:18441236 | pubmed:author | pubmed-author:AtlasAnnA | lld:pubmed |
pubmed-article:18441236 | pubmed:author | pubmed-author:FluurCaroline... | lld:pubmed |
pubmed-article:18441236 | pubmed:author | pubmed-author:RuffinNicolas... | lld:pubmed |
pubmed-article:18441236 | pubmed:author | pubmed-author:VivarNancyN | lld:pubmed |
pubmed-article:18441236 | pubmed:author | pubmed-author:SammicheliSte... | lld:pubmed |
pubmed-article:18441236 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:18441236 | pubmed:day | 15 | lld:pubmed |
pubmed-article:18441236 | pubmed:volume | 112 | lld:pubmed |
pubmed-article:18441236 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18441236 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18441236 | pubmed:pagination | 1195-204 | lld:pubmed |
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pubmed-article:18441236 | pubmed:meshHeading | pubmed-meshheading:18441236... | lld:pubmed |
pubmed-article:18441236 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18441236 | pubmed:articleTitle | Priming of T cells to Fas-mediated proliferative signals by interleukin-7. | lld:pubmed |
pubmed-article:18441236 | pubmed:affiliation | Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden. | lld:pubmed |
pubmed-article:18441236 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18441236 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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