Abstract
TCR-mediated activation of T cell hybridomas induces programmed cell death by a Fas-dependent pathway. We now show that costimulation of 2B4 cells, in the absence or presence of transgenic Bcl-2, with anti-CD3ε and forskolin, an activator of cAMP signaling, resulted in antagonism of Fas-dependent activation-induced cell death that was always accompanied by selective down-regulation of the nuclear levels of NF-κB p65-p50 (RelA-p50) transcription factor. Forskolin not only inhibited activation-induced cell death and NF-κB activation, but also suppressed expression of Fas and Fas ligand (Fas-L). Furthermore, NF-κB p65 antisense oligonucleotide down-regulated nuclear levels of NF-κB, inhibited cell surface expression of Fas-L and apoptosis of 2B4. Collectively, these finding demonstrate a potential role of NF-κB in the regulation of activation-induced apoptosis in T lymphocytes.
Original language | English (US) |
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Pages (from-to) | 2455-2464 |
Number of pages | 10 |
Journal | Oncogene |
Volume | 14 |
Issue number | 20 |
DOIs | |
State | Published - 1997 |
Keywords
- Apoptosis
- Fas ligand
- NF-κB
- T lymphocyte
ASJC Scopus subject areas
- Molecular Biology
- Cancer Research
- Genetics