期刊
CELL DEATH AND DIFFERENTIATION
卷 15, 期 2, 页码 354-363出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/sj.cdd.4402264
关键词
NF-kappa B; p73; apoptosis; costimulation; memory T cells
资金
- Associazione Italiana per la Ricerca sul Cancro Funding Source: Custom
The balance between antiapoptotic and proapoptotic proteins of the Bcl-2 family is critical in determining the fate of T cells in response to death stimuli. Proapoptotic genes, such as bax, are generally regulated by the p53 family of transcription factors, whereas NF-kappa B subunits can activate the transcription of antiapoptotic Bcl-2 members. Here, we show that CD28 activation protects memory T cells from irradiation-induced apoptosis by both upregulating bcl-xL and inhibiting bax gene expression. We found that p73, but not p53, binds to and trans-activates the bax gene promoter in irradiated T cells. The activation of RelA/NF-kappa B subunit in CD28 costimulated T cells and its binding onto the bax gene promoter results in suppression of bax transcription and decrease in both p73 and RNA polymerase II recruitment in vivo. RelA recruitment on the bax gene promoter is also accompanied by the lost of p300 binding and the parallel appearance of histone deacetylase-1-containing complexes. These findings identify RelA/NF-kappa B as a critical regulator of T-cell survival by affecting the balance of Bcl-2 family members.
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