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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Reversal of functional defects in highly differentiated young and old CD8 T cells by PDL blockade
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Reversal of functional defects in highly differentiated young and old CD8 T cells by PDL blockade

机译：通过PDL阻断逆转高分化年轻和老CD8 T细胞的功能缺陷

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摘要

Highly differentiated CD8 +CD28 -CD27 - T cells have short telomeres, defective telomerase activity and reduced capacity for proliferation. In addition, these cells express increased levels of inhibitory receptors and display defective Akt(ser 473) phosphorylation following activation. It is not known whether signalling via programmed death 1 (PD-1) contributes to any of the attenuated differentiation-related functional changes in CD8 + T cells. To address this we blocked PD-1 signalling during T-cell receptor (TCR) activation using antibodies against PD-1 ligand 1 (PDL1) and PDL2. This resulted in a significant enhancement of Akt(ser 473) phosphorylation and TCR-induced proliferative activity of highly differentiated CD8 +CD28 -CD27 - T cells. In contrast, the reduced telomerase activity in these cells was not altered by blockade of PDL1/2. We also demonstrate that PD-1 signalling can inhibit the proliferative response in primary human CD8 + T cells from both young and older humans. These data collectively highlight that some, but not all, functional changes that arise during progressive T-cell differentiation and during ageing are maintained actively by inhibitory receptor signalling.
机译：高分化的CD8 + CD28 -CD27-T细胞端粒短，端粒酶活性低和增殖能力降低。此外，这些细胞表达增加水平的抑制受体，并在激活后显示缺陷的Akt（ser 473）磷酸化。尚不知道通过程序性死亡1（PD-1）发出的信号是否会导致CD8 + T细胞中任何与分化相关的功能减弱。为了解决这个问题，我们使用针对PD-1配体1（PDL1）和PDL2的抗体在T细胞受体（TCR）激活过程中阻断了PD-1信号传导。这导致Akt（ser 473）磷酸化和TCR诱导的高分化CD8 + CD28 -CD27-T细胞的增殖活性显着增强。相反，在这些细胞中降低的端粒酶活性并未因PDL1 / 2的阻断而改变。我们还证明了PD-1信号传导可以抑制年轻人和老年人的原代人CD8 + T细胞中的增殖反应。这些数据共同突出表明，在进行性T细胞分化过程中和衰老过程中出现的一些（但不是全部）功能变化通过抑制性受体信号传导得以积极维持。

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