Effector and memory CD8+ T cell fate coupled by T-bet and eomesodermin
Effector and memory CD8+ T cell fate coupled by T-bet and eomesodermin
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DOI：
10.1038/ni1268
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发表时间：
2005-12-01
影响因子：
30.5
通讯作者：
Reiner, SL
中科院分区：
文献类型：
--
作者：
Intlekofer, AM;Takemoto, N;Reiner, SL
记忆CD8（+）T细胞的两个看似无关的标志是病原体清除率后细胞因子驱动的增生性更新和一个潜在的效应程序，以期预期获得。记忆CD8（+）T细胞和天然杀伤细胞具有细胞毒性潜力和对生长因子白细胞介素15的依赖性。我们现在表明，具有转录因子T-bet和Eomesodermin的基因复合突变的小鼠几乎没有依赖于几个谱系的小鼠在白介素15上，包括记忆CD8（+）T细胞和成熟的天然杀伤细胞，并且它们的细胞具有缺陷的细胞毒性效应子编程。此外，T-bet和Eomesodermin负责诱导CD122的增强表达，这是指定白介素15反应性的受体。因此，这些关键转录因子将记忆CD8（+）T细胞的长期更新与其特征效应效力联系起来。
Two seemingly unrelated hallmarks of memory CD8(+) T cells are cytokine-driven proliferative renewal after pathogen clearance and a latent effector program in anticipation of rechallenge. Memory CD8(+) T cells and natural killer cells share cytotoxic potential and dependence on the growth factor interleukin 15. We now show that mice with compound mutations of the genes encoding the transcription factors T-bet and eomesodermin were nearly devoid of several lineages dependent on interleukin 15, including memory CD8(+) T cells and mature natural killer cells, and that their cells had defective cytotoxic effector programming. Moreover, T-bet and eomesodermin were responsible for inducing enhanced expression of CD122, the receptor specifying interleukin 15 responsiveness. Therefore, these key transcription factors link the long-term renewal of memory CD8(+) T cells to their characteristic effector potency.