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Blood, 15 August 2008, Vol. 112, No. 4, pp. 1195-1204. Prepublished online as a Blood First Edition Paper on April 25, 2008; DOI 10.1182/blood-2007-12-126698. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2007-12-126698v1 112/4/1195    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Rethi, B. Articles by Chiodi, F. Search for Related Content PubMed PubMed Citation Articles by Rethi, B. Articles by Chiodi, F. Related Collections Immunobiology Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY Priming of T cells to Fas-mediated proliferative signals by interleukin-7 Bence Rethi1,2,*, Nancy Vivar1,*, Stefano Sammicheli1, Caroline Fluur1, Nicolas Ruffin1, Ann Atlas3, Eva Rajnavolgyi2, and Francesca Chiodi1 1 Department of Microbiology, Tumor and Cell Biology, Karolinska Institutet, Stockholm, Sweden; 2 Institute of Immunology, Medical and Health Science Center, Faculty of Medicine, University of Debrecen, Debrecen, Hungary; and 3 Infectious Diseases Unit, Department of Medicine and Karolinska University Hospital, Solna, Sweden 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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Fas, IL-7, and T cells: live and let die Franco Lori Blood 2008 112: 930-931. [Full Text] [PDF]

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