Vγ9Vδ2 T-cells play a key role in the innate immune response to viral infections through butyrophilin (BTN)-3A. Here, we reported that blood Vγ9Vδ2 T-cells decreased in clinically mild COVID-19 compared to healthy volunteers (HV), and was maintained up to 28-days and in the recovery period. Terminally differentiated Vγ9Vδ2 T-cells tend to be enriched on the day of diagnosis, 28-days after and during the recovery period. These cells showed cytotoxic and inflammatory activities following anti-BTN3A activation. BTN3A upregulation and Vγ9Vδ2 T-cell infiltration were observed in a lung biopsy from a fatal SARS-CoV-2 infection. In vitro, SARS-CoV-2 infection increased BTN3A expression in macrophages and lung cells that enhanced the anti-SARS-CoV-2 Vγ9Vδ2 T-cells cytotoxicity and IFNγ and TNFα. Increasing concentrations of anti-BTN3A lead to viral replication inhibition. Altogether, we report that Vγ9Vδ2 T-cells are important in the immune response against SARS-CoV-2 infection and that activation by an anti-BTN3A antibody may enhance their response.

中文翻译：

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Vγ9Vδ2 T 细胞是 SARS-CoV-2 复制的有效抑制剂，代表了 COVID-19 患者的效应表型

Vγ9Vδ2 T 细胞通过嗜丁酸蛋白 (BTN)-3A 在针对病毒感染的先天免疫反应中发挥关键作用。在这里，我们报告说，与健康志愿者 (HV) 相比，临床轻度 COVID-19 中的血液 Vγ9Vδ2 T 细胞减少，并维持长达 28 天和恢复期。终末分化的 Vγ9Vδ2 T 细胞往往在诊断当天、诊断后 28 天以及恢复期间富集。这些细胞在抗 BTN3A 激活后表现出细胞毒性和炎症活性。在致命 SARS-CoV-2 感染的肺活检中观察到 BTN3A 上调和 Vγ9Vδ2 T 细胞浸润。在体外，SARS-CoV-2感染增加了巨噬细胞和肺细胞中BTN3A的表达，从而增强了抗SARS-CoV-2 Vγ9Vδ2 T细胞的细胞毒性以及IFNγ和TNFα。抗 BTN3A 浓度的增加会导致病毒复制受到抑制。总之，我们报告 Vγ9Vδ2 T 细胞在针对 SARS-CoV-2 感染的免疫反应中很重要，并且抗 BTN3A 抗体的激活可能会增强其反应。