Review
Version 1
Preserved in Portico This version is not peer-reviewed
The Functional Roles of MDSCs in Severe COVID-19 Pathogenesis
Version 1
: Received: 18 November 2023 / Approved: 21 November 2023 / Online: 23 November 2023 (11:18:17 CET)
A peer-reviewed article of this Preprint also exists.
Len, J.S.; Koh, C.W.T.; Chan, K.R. The Functional Roles of MDSCs in Severe COVID-19 Pathogenesis. Viruses 2024, 16, 27. Len, J.S.; Koh, C.W.T.; Chan, K.R. The Functional Roles of MDSCs in Severe COVID-19 Pathogenesis. Viruses 2024, 16, 27.
Abstract
Severe COVID-19 is a major cause of morbidity and mortality worldwide, especially to those with co-morbidities, the elderly and the immunocompromised. However, the molecular determinants critical for severe COVID-19 progression remain to be fully elucidated. Meta-analysis of transcriptomic RNAseq and single-cell sequencing datasets comparing between severe and mild COVID-19 patients have demonstrated that the early expansion of myeloid-derived suppressor cells (MDSCs) could a key feature of severe COVID-19 progression. Besides serving as potential early prognostic biomarkers for severe COVID-19 progression, several studies have also indicated the functional roles of MDSCs in severe COVID-19 pathogenesis and possibly even long COVID. Given the potential links between MDSCs and severe COVID-19, we examined the existing literature summarizing the characteristics of MDSCs, the evidence of MDSCs in facilitating severe COVID-19 pathogenesis and discuss the potential therapeutic avenues that can be explored to reduce the risk and burden of severe COVID-19. We also provide a web app where users can visualise the temporal changes of specific genes or MDSC-related gene sets during severe COVID-19 progression and disease resolution at https://temporal-severe-covid.streamlit.app/, based on our previous study described by Ong et al., 2021.
Keywords
SARS-CoV-2; COVID-19; myeloid-derived suppressor cells; infection; innate immunity; T cells
Subject
Biology and Life Sciences, Virology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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