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* Laboratory of Immunology,
Département de Microbiologie et d’Immunologie and
Centre de Recherche du Centre Hospitalier de l’Université de Montréal, and
Département de Médecine, Université de Montréal, Montreal, Canada;
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Department of Microbiology and Immunology and
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Faculty of Medicine, Division of Experimental Medicine, McGill University, Montreal, Canada;
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Guy-Bernier Research Center, Maisonneuve-Rosemont Hospital, Montreal, Canada;
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Emory Vaccine Center, Emory University School of Medicine, Atlanta, GA 30322; and
Ontario Cancer Institute, Department of Medicine, University of Toronto, Toronto, Canada
Caspases play a central role in T lymphocyte activation and death. We have demonstrated previously that caspase-3, an effector molecule for activation-induced cell death (AICD), is processed following T cell activation in the absence of apoptosis. We report in this study that caspase-3 mRNA levels were selectively increased in peripheral T cells, following Ag receptor-mediated activation. The up-regulation of caspase-3 mRNA was confined to cells in the early phases of the cell cycle (G0/G1) and was independent of IL-2 signaling. This increase led to the renewal of procaspase-3 as evidenced by a 6-fold up-regulation of the zymogen in nonapoptotic stimulated T cells. The increase of mRNA levels and of both the zymogen and the cleaved forms of caspase-3 was observed in in vivo stimulated Ag-specific effector, but not memory T cells, correlating with the enhanced susceptibility of effector T cells to AICD. Furthermore, we confirm that caspase-3 levels directly influence the sensitivity of activated T cells to apoptosis, as shown using T lymphocytes isolated from caspase-3 heterozygous and knockout mice. These findings indicate that the selective up-regulation of caspase-3 transcription is required to maintain the cytoplasmic levels of this protease, which control AICD and T cell homeostasis.
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