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RelA regulates the survival of activated effector CD8 T cells.

机译:RelA调节活化的效应CD8 T细胞的存活。

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Nuclear factor of kappa B (NF-kappaB) transcription factors are critical regulators of T-cell activation and survival. The relative contribution of individual NF-kappaB 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 kappaB 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.
机译:核转录因子κB(NF-kappaB)是T细胞活化和存活的关键调节因子。各个NF-κB成员对这些过程的相对贡献仍然难以捉摸。我们研究了RelA在调节CD8 T细胞活化中的作用。我们在成熟的CD8 T细胞中过度表达了一个反激活域缺陷的RelA分子(p65TAD)。我们表明p65TAD形成同kappaB位点并选择性抑制RelA依赖性反式激活的p50的同型和异型二聚体。 p65TAD的表达不影响初始激活或细胞周期进程,但可在体外和体内诱导活化的CD8 T细胞死亡。但是,静止的效应CD8 T细胞的长期存活似乎不受p65TAD表达的影响。总体而言,我们的结果表明,RelA是增殖CD8 T细胞存活的关键调节剂,但对于静息效应T细胞的存活可能是必不可少的。

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