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-κB 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-K15-dependent antiapoptotic genes were expressed with kinetics that paralleled nuclear expression of p65/RelA. Of these three, ectopic expression only of Gadd45β protected significantly against AICD, whereas IEX-1 and Bcl-X, were much less effective. VVe 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.
|Original language||English (US)|
|Number of pages||7|
|Journal||Journal of Immunology|
|State||Published - Feb 15 2006|
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