| First Author | Mittal A | Year | 2006 |
| Journal | J Immunol | Volume | 176 |
| Issue | 4 | Pages | 2183-9 |
| PubMed ID | 16455974 | Mgi Jnum | J:129121 |
| Mgi Id | MGI:3768713 | Doi | 10.4049/jimmunol.176.4.2183 |
| Citation | Mittal A, et al. (2006) NF-kappaB-dependent regulation of the timing of activation-induced cell death of T lymphocytes. J Immunol 176(4):2183-9 |
| abstractText | 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-kappaB 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-kappaB-dependent antiapoptotic genes were expressed with kinetics that paralleled nuclear expression of p65/RelA. Of these three, ectopic expression only of Gadd45beta 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. |
