RelA regulates the survival of activated effector CD8 T cells

被引:0
作者
I Mondor
A-M Schmitt-Verhulst
S Guerder
机构
[1] Centre d'Immunologie de Marseille-Luminy,
[2] Institut National de la Santé et de la Recherche Médicale/Centre National de la Recherche Scientifique/Université de la Méditerranée,undefined
[3] Parc Scientifique de Luminy,undefined
来源
Cell Death & Differentiation | 2005年 / 12卷
关键词
T lymphocytes; transcription factors; cellular activation; cellular proliferation; memory;
D O I
暂无
中图分类号
学科分类号
摘要
Nuclear factor of kappa B (NF-κB) transcription factors are critical regulators of T-cell activation and survival. The relative contribution of individual NF-κB members to these processes remains elusive. We investigated the role of RelA in the regulation of CD8 T-cell activation. We overexpressed, in mature CD8 T cells, a transactivation domain-deficient RelA molecule (p65TAD). We show that p65TAD forms homo- and heterodimers with p50 that bind κB sites and selectively inhibit RelA-dependent transactivation. Expression of p65TAD does not affect initial activation or cell cycle progression but induces the death of activated CD8 T cells in vitro and in vivo. However, the long-term survival of resting effector CD8 T cells seems not to be affected by p65TAD expression. Collectively, our results indicate that RelA is a critical regulator of survival of proliferating CD8 T cells but may be dispensable for the survival of resting effector T cells.
引用
收藏
页码:1398 / 1406
页数:8
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