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Blood, 1 July 2004, Vol. 104, No. 1, pp. 215-223. Prepublished online as a Blood First Edition Paper on March 18, 2004; DOI 10.1182/blood-2003-12-4295. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-12-4295v1 104/1/215    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Asselin-Labat, M.-L. Articles by Pallardy, M. Search for Related Content PubMed PubMed Citation Articles by Asselin-Labat, M.-L. Articles by Pallardy, M. Related Collections Immunobiology Apoptosis Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  IMMUNOBIOLOGY GILZ, a new target for the transcription factor FoxO3, protects T lymphocytes from interleukin-2 withdrawal–induced apoptosis Marie-Liesse Asselin-Labat, Muriel David, Armelle Biola-Vidamment, Damiana Lecoeuche, Maria-Christina Zennaro, Jacques Bertoglio, and Marc Pallardy From the Institut National de la Santé et de la Recherche Médicale (INSERM) U 461, Faculté de Pharmacie Paris XI, Châtenay-Malabry, France; and INSERM U 478, Faculté deMédecine X. Bichat, Paris, France. Interleukin-2 (IL-2) withdrawal is a physiologic process inducing cell death in activated T lymphocytes. Glucocorticoid-induced leucine zipper (GILZ) has recently been identified as a protein modulating T-cell receptor activation by repressing various signaling pathways. We report here that IL-2 deprivation leads to expression of GILZ in T lymphocytes. We then characterized the human gilz promoter and showed that FoxO3 (Forkhead box class O3) binding to the Forkhead responsive elements identified in the promoter is necessary for induction of gilz expression upon IL-2 withdrawal. To assess the functional consequences of this induction, we used 2 strategies, GILZ overexpression and GILZ silencing in murine IL-2–dependent CTLL-2 cells. GILZ overexpression protects CTLL-2 cells from IL-2 withdrawal–induced apoptosis, whereas cell death is accelerated in cells unable to express GILZ. Concomitantly, the expression of Bim is inhibited in GILZ-overexpressing cells and enhanced when GILZ expression is impaired. Furthermore, GILZ inhibits FoxO3 transcriptional activity that leads to inhibition of Bim expression but also to down-regulation of GILZ itself. Therefore, GILZ is a transiently expressed protein induced upon IL-2 withdrawal that protects T cells from the onset of apoptosis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. Cui, Y. Huang, Y. Zhao, and J. Zheng Transcription Factor FOXO3a Mediates Apoptosis in HIV-1-Infected Macrophages J. Immunol., January 15, 2008; 180(2): 898 - 906. [Abstract] [Full Text] [PDF] R. Soundararajan, J. Wang, D. Melters, and D. Pearce Differential Activities of Glucocorticoid-induced Leucine Zipper Protein Isoforms J. Biol. Chem., December 14, 2007; 282(50): 36303 - 36313. [Abstract] [Full Text] [PDF] H. Hamdi, V. Godot, M.-C. Maillot, M. V. Prejean, N. Cohen, R. Krzysiek, F. M. Lemoine, W. Zou, and D. Emilie Induction of antigen-specific regulatory T lymphocytes by human dendritic cells expressing the glucocorticoid-induced leucine zipper Blood, July 1, 2007; 110(1): 211 - 219. [Abstract] [Full Text] [PDF] W. J. 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