Recent studies have implicated the cell surface receptor Programmed Death-1 (PD-1) in numerous models of T cell anergy, though the specific mechanisms by which the PD-1 signal maintains tolerance is not clear. We demonstrate that the depletion of PD-1 with siRNA results in a complete reversal of clonal anergy in the A.E7 T cell model, suggesting that the mechanism by which PD-1 maintains the anergic phenotype is a T-cell-intrinsic phenomenon, and not one dependent on other cell populations in vivo. We have also shown that the neutralization of IL-2 during restimulation abrogates the effect of PD-1 depletion, suggesting that tolerance mediated by PD-1 is wholly IL-2 dependent, and likewise intrinsic to the tolerized cells.

中文翻译：

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程序性死亡 1 受体的耗竭完全逆转了 CD4(+) T 淋巴细胞通过白介素 2 依赖性机制建立的克隆性无反应性。

最近的研究表明，细胞表面受体程序性死亡 1 (PD-1) 与许多 T 细胞无反应性模型有关，尽管 PD-1 信号维持耐受性的具体机制尚不清楚。我们证明 PD-1 与 siRNA 的消耗导致 A.E7 T 细胞模型中克隆无反应性的完全逆转，表明 PD-1 维持无反应性表型的机制是 T 细胞内在现象，而不是依赖于体内其他细胞群。我们还表明，再刺激过程中 IL-2 的中和消除了 PD-1 耗竭的影响，表明 PD-1 介导的耐受完全依赖于 IL-2，并且同样是耐受细胞所固有的。