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The cysteine protease interleukin-1beta converting enzyme (ICE) is implicated as an effector of apoptosis in mammalian cells. Proteolytic activity of ICE can be blocked in vitro by the cytokine response modifier A (crmA), a serpin-like protease inhibitor encoded by cowpox virus. Here we show that CD2 enhancer-driven expression of crmA in T lymphocytes of transgenic mice (CD2-crmA mice) reduces CD95 (Fas/APO-1)-transduced apoptosis in vitro to the level seen in CD95-deficient mutant lpr mice, but does not protect against gamma-radiation or corticosteroid-induced cell death. Unlike lpr mice, CD2-crmA transgenic mice developed neither T cell hyperplasia nor serum autoantibodies. These results provide evidence that the phenotype of lpr mice is not simply due to failure of CD95 to trigger T cell apoptosis mediated by ICE.


Journal article



Publication Date





5167 - 5176


Animals, Apoptosis, Autoantibodies, CD2 Antigens, Cell Survival, Cells, Cultured, Dexamethasone, Enhancer Elements, Genetic, Gamma Rays, Gene Expression, Glucocorticoids, Humans, Lymph Nodes, Lymphocyte Activation, Mice, Mice, Mutant Strains, Mice, Transgenic, Proto-Oncogene Proteins c-bcl-2, RNA, Messenger, Receptors, Antigen, T-Cell, alpha-beta, Serpins, Spleen, T-Lymphocytes, Thy-1 Antigens, Thymus Gland, Viral Proteins, fas Receptor