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 Blood, 15 February 2007, Vol. 109, No. 4, pp. 1627-1635.
Prepublished online as a Blood First Edition Paper on October 24, 2006; DOI 10.1182/blood-2006-05-022319.

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IMMUNOBIOLOGY

The induction of Bim expression in human T-cell blasts is dependent on nonapoptotic Fas/CD95 signaling

Alberto Bosque1, Juan Ignacio Aguiló1, M. Angeles Alava1, Estela Paz-Artal2, Javier Naval1, Luis M. Allende2, and Alberto Anel1

1 Departamento de Bioquímica y Biología Molecular y Celular, Facultad de Ciencias, Universidad de Zaragoza, Spain; 2 Servicio de Inmunología, Hospital 12 de Octubre, Madrid, Spain

The BH3-only protein Bim is required for maintaining the homeostasis of the immune system, since Bim regulates the down-modulation of T-cell responses, mainly through cytokine deprivation. Using T-cell blasts from healthy donors and also from patients with autoimmune lymphoproliferative syndromes (ALPSs) due to homozygous loss-of-function mutation of FasL (ALPS-Ic) or heterozygous mutation in the Fas/CD95 death domain (ALPS-Ia), it is shown that the induction of Bim expression during the process of human T-cell blast generation is strictly dependent on FasL/Fas-mediated signaling. The main pathway by which Fas signaling regulates the levels of Bim expression in human T-cell blasts is the death-domain– and caspase-independent generation of discrete levels of H2O2, which results in the net increase of Foxo3a levels. The present results connect the 2 main pathways described until the moment for the control of T-cell responses: death receptor–mediated activation-induced cell death and apoptosis by cytokine deprivation.


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This article has been cited by other articles:


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 J. Leukoc. Biol.Home page
A. Bosque, J. I. Aguilo, M. del Rey, E. Paz-Artal, L. M. Allende, J. Naval, and A. Anel
Cell cycle regulation by FasL and Apo2L/TRAIL in human T-cell blasts. Implications for autoimmune lymphoproliferative syndromes
J. Leukoc. Biol., August 1, 2008; 84(2): 488 - 498.
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