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Enhancing Siv-specific Immunity In Vivo By Pd-1 Blockade

机译：通过Pd-1封锁增强Siv的体内免疫力

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Chronic immunodeficiency virus infections are characterized by dysfunctional cellular and humoral antiviral immune responses. As such, immune modulatory therapies that enhance and/or restore the function of virus-specific immunity may protect from disease progression. Here we investigate the safety and immune restoration potential of blockade of the co-inhibitory receptor programmed death 1 (PD-1) during chronic simian immunodeficiency virus (SIV) infection in macaques. We demonstrate that PD-1 blockade using an antibody to PD-1 is well tolerated and results in rapid expansion of virus-specific CD8 T cells with improved functional quality. This enhanced T-cell immunity was seen in the blood and also in the gut, a major reservoir of SIV infection. PD-1 blockade also resulted in proliferation of memory B cells and increases in SIV envelope-specific antibody. These improved immune responses were associated with significant reductions in plasma viral load and also prolonged the survival of SIV-infected macaques. Blockade was effective during the early (week 10) as well as late (～week 90) phases of chronic infection even under conditions of severe lymphopenia. These results demonstrate enhancement of both cellular and humoral immune responses during a pathogenic immunodeficiency virus infection by blocking a single inhibitory pathway and identify a novel therapeutic approach for control of human immunodeficiency virus infections.
机译：慢性免疫缺陷病毒感染的特征是细胞和体液抗病毒免疫功能异常。这样，增强和/或恢复病毒特异性免疫功能的免疫调节疗法可以防止疾病进展。在这里，我们研究了猕猴慢性猿猴免疫缺陷病毒（SIV）感染期间共抑制受体编程性死亡1（PD-1）的阻断的安全性和免疫修复潜力。我们证明使用PD-1抗体对PD-1的阻滞作用耐受良好，并会导致病毒特异性CD8 T细胞快速扩增，功能质量得到改善。在血液和肠道（SIV感染的主要储存库）中都可以看到这种增强的T细胞免疫力。 PD-1阻断还导致记忆B细胞增殖，并增加SIV包膜特异性抗体。这些改善的免疫反应与血浆病毒载量的显着降低有关，也延长了被SIV感染的猕猴的存活时间。即使在严重的淋巴细胞减少症的情况下，封锁在慢性感染的早期（第10周）和晚期（〜90周）均有效。这些结果表明，通过阻断单一抑制途径，在致病性免疫缺陷病毒感染过程中细胞和体液免疫应答均得到增强，并确定了控制人类免疫缺陷病毒感染的新型治疗方法。

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