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PD-1 表达上调和高 sPD-L1 水平与 COVID-19 严重程度相关。

Upregulation of PD-1 Expression and High sPD-L1 Levels Associated with COVID-19 Severity.

机构信息

Laboratory of Dermatology and Immunodeficiencies, LIM 56, Tropical Medicine Institute, School of Medicine, University of Sao Paulo, Brazil.

Department of Dermatology, Faculdade de Medicina FMUSP, Universidade de Sao Paulo, 01246-903 Sao Paulo, Brazil.

出版信息

J Immunol Res. 2022 Aug 1;2022:9764002. doi: 10.1155/2022/9764002. eCollection 2022.

DOI:10.1155/2022/9764002
PMID:35971391
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9375698/
Abstract

COVID-19 has several mechanisms that can lead to lymphocyte depletion/exhaustion. The checkpoint inhibitor molecule programmed death protein 1 (PD-1) and its programmed death-ligand 1 (PDL-1) play an important role in inhibiting cellular activity as well as the depletion of these cells. In this study, we evaluated PD-1 expression in TCD4+, TCD8+, and CD19+ lymphocytes from SARS-CoV-2-infected patients. A decreased frequency of total lymphocytes and an increased PD-1 expression in TCD4+ and CD19+ lymphocytes were verified in severe/critical COVID-19 patients. In addition, we found a decreased frequency of total monocytes with an increased PD-1 expression on CD14+ monocytes in severe/critical patients in association with the time of infection. Moreover, we observed an increase in sPD-L1 circulant levels associated with the severity of the disease. Overall, these data indicate an important role of the PD-1/PDL-1 axis in COVID-19 and may provide a severity-associated biomarker and therapeutic target during SARS-CoV-2 infection.

摘要

COVID-19 有几种机制可导致淋巴细胞耗竭/衰竭。检查点抑制剂分子程序性死亡蛋白 1(PD-1)及其程序性死亡配体 1(PDL-1)在抑制细胞活性以及这些细胞耗竭方面发挥着重要作用。在这项研究中,我们评估了 SARS-CoV-2 感染患者的 TCD4+、TCD8+和 CD19+淋巴细胞中的 PD-1 表达。在重症/危重症 COVID-19 患者中,证实总淋巴细胞频率降低,TCD4+和 CD19+淋巴细胞中 PD-1 表达增加。此外,我们还发现重症/危重症患者中总单核细胞频率降低,CD14+单核细胞上 PD-1 表达增加,且与感染时间有关。此外,我们还观察到与疾病严重程度相关的 sPD-L1 循环水平升高。总的来说,这些数据表明 PD-1/PDL-1 轴在 COVID-19 中的重要作用,并且可能为 SARS-CoV-2 感染期间提供与严重程度相关的生物标志物和治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8680/9375698/be6dde0b9583/JIR2022-9764002.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8680/9375698/236a93a8445b/JIR2022-9764002.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8680/9375698/b36058137a46/JIR2022-9764002.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8680/9375698/be6dde0b9583/JIR2022-9764002.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8680/9375698/236a93a8445b/JIR2022-9764002.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8680/9375698/b36058137a46/JIR2022-9764002.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8680/9375698/be6dde0b9583/JIR2022-9764002.003.jpg

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