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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.
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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.
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