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Targeting the programmed cell death 1: programmed cell death ligand 1 pathway reverses T cell exhaustion in patients with sepsis

机译:靶向程序性细胞死亡1:程序性细胞死亡配体1途径可逆转败血症患者的T细胞衰竭

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摘要

IntroductionA major pathophysiologic mechanism in sepsis is impaired host immunity which results in failure to eradicate invading pathogens and increased susceptibility to secondary infections. Although many immunosuppressive mechanisms exist, increased expression of the inhibitory receptor programmed cell death 1 (PD-1) and its ligand (PD-L1) are thought to play key roles. The newly recognized phenomenon of T cell exhaustion is mediated in part by PD-1 effects on T cells. This study tested the ability of anti-PD-1 and anti-PD-L1 antibodies to prevent apoptosis and improve lymphocyte function in septic patients.
机译:引言败血症的主要病理生理机制是宿主免疫力受损,导致无法根除入侵的病原体并增加了对继发感染的易感性。尽管存在许多免疫抑制机制,但抑制受体编程性细胞死亡1(PD-1)及其配体(PD-L1)的表达增加被认为起关键作用。新认识到的T细胞衰竭现象部分由PD-1对T细胞的影响介导。这项研究测试了抗PD-1和抗PD-L1抗体预防败血病患者凋亡和改善淋巴细胞功能的能力。

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