CrmA expression in T lymphocytes of transgenic mice inhibits CD95 (Fas/APO-1)-transduced apoptosis, but does not cause lymphadenopathy or autoimmune disease
- Author(s)
- Smith, KGC; Strasser, A; Vaux, DL;
- Details
- Publication Year 1996-10-01,Volume 15,Issue #19,Page 5167-5176
- Journal Title
- EMBO JOURNAL
- Publication Type
- Journal Article
- Abstract
- The cysteine protease interleukin-1 beta converting enzyme (ICE) is implicated as an effector of apoptosis in mammalian cells. Proteolytic activity of ICE can be blocked in vitro by the cgtokine response modifier A (crmA), a serpin-like protease inhibitor encoded by cow-pox 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.
- Publisher
- OXFORD UNIV PRESS UNITED KINGDOM
- Keywords
- TUMOR NECROSIS FACTOR; DEATH GENE CED-3; INTERLEUKIN-1-BETA CONVERTING-ENZYME; ACTIVATION-INDUCED APOPTOSIS; PROGRAMMED CELL-DEATH; IL-1-BETA-CONVERTING ENZYME; COWPOX VIRUS; FAS-LIGAND; LYMPHOPROLIFERATIVE DISEASE; CAENORHABDITIS-ELEGANS
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- Refer to copyright notice on published article.
Creation Date: 1996-10-01 12:00:00