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NF-B-Dependent Regulation of the Timing of Activation-Induced Cell Death of T Lymphocytes¹

Akanksha Mittal^*, Salvatore Papa, Guido Franzoso and Ranjan Sen^2,

^* Rosensteil Research Center and Department of Biology, Brandeis University, Waltham, MA 02454; Laboratory of Cellular and Molecular Biology, National Institute on Aging, Baltimore, MD 21224; and Ben May Institute for Cancer Research, University of Chicago, Chicago, IL 60637

One of the mechanisms by which activated T cells die is activation-induced cell death (AICD). This pathway requires persistent stimulation via the TCR and engagement of death receptors. We found that TCR stimulation led to transient nuclear accumulation of the NF-B component p65/RelA. In contrast, nuclear c-Rel levels remained high even after extended periods of activation. Loss of nuclear p65/RelA correlated with the onset of AICD, suggesting that p65/RelA target genes may maintain cell viability. Quantitative RNA analyses showed that three of several putative NF-B-dependent antiapoptotic genes were expressed with kinetics that paralleled nuclear expression of p65/RelA. Of these three, ectopic expression only of Gadd45 protected significantly against AICD, whereas IEX-1 and Bcl-x_L were much less effective. We propose that the timing of AICD, and thus the length of the effector phase, are regulated by transient expression of a subset of p65/RelA-dependent antiapoptotic genes.

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