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The Journal of Immunology, Vol 155, Issue 7 3433-3442, Copyright © 1995 by American Association of Immunologists
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JP Vasilakos, T Ghayur, RT Carroll, DA Giegel, JM Saunders, L Quintal, KM Keane and BD Shivers
Neuroscience Therapeutics, Parke-Davis Pharmaceutical Research Company, Ann Arbor, MI 48105, USA.
Clonal T cells undergo programmed cell death (PCD) or apoptosis when cultured without the appropriate cytokines. The cysteine protease, IL-1 beta converting enzyme (ICE), is implicated in apoptosis based on its structural similarity to the PCD gene, ced-3, in Caenorhabditis elegans and the induction of PCD in fibroblasts transfected with recombinant ICE. We show that the murine IL-2-dependent CTLL T cell line expresses ICE but not IL-1 beta. Interestingly, ICE mRNA and protein levels increase during apoptosis. Yet inhibition of ICE enzymatic activity (> 90%) with either of two cell-permeable ICE inhibitors does not abrogate or delay apoptosis following IL-2 deprivation, as measured by DNA fragmentation and viability. Our results suggest that ICE is not required for apoptosis in lymphokine-deprived T cells.
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