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The Journal of Immunology, Vol 156, Issue 11 4075-4078, Copyright © 1996 by American Association of Immunologists
CUTTING EDGE |
SA Boehme and MJ Lenardo
Laboratory of Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
The p53 protein plays an important role in various forms of thymocyte apoptosis, however its role in mature T lymphocyte death caused by TCR stimulation has not been examined. We demonstrate here that T cell blasts derived from mice containing a germ-line deficiency of the p53 tumor suppressor gene are susceptible to TCR-induced apoptosis to the same degree as wild-type T cells. TCR stimulation of both resting and proliferatingT cells results in up-regulated expression of the p53- induced genes Bax and p21, and the induction of these genes appears reduced in T cells that are deficient in p53. Thus, while activation of p53-dependent genes following TCR stimulation is defective in p53-/- T cells, there is no impairment in their ability to undergo apoptosis. These results suggest that TCR-mediated apoptosis of mature T cells takes place via a pathway that is independent of p53.
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