PMC:7200337 / 13704-15434 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7200337","sourcedb":"PMC","sourceid":"7200337","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7200337","text":"Myeloid Characterization in COVID-19\nFlow cytometric analyses of peripheral blood mononuclear cells (PBMCs) from symptomatic COVID-19 patients have shown a significant influx of granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing, activated CD4+ T cells and CD14+HLA-DRlo inflammatory monocytes (IMs) (Giamarellos-Bourboulis et al., 2020, Zhang et al., 2020c, Zhou et al., 2020b). This matches single-cell transcriptomic (scRNA-seq) data demonstrating CD14+IL-1β+ monocytic expansion (Guo et al., 2020, Wen et al., 2020), interferon-mitogen-activated protein kinase (MAPK)-driven adaptive immune responses (Huang et al., 2020c), and IL-1β-associated inflammasome signatures (Ong et al., 2020) in peripheral blood of COVID-19 patients, although systemic levels of IL-1β detected are conspicuously low (Del Valle et al., 2020). Importantly, these immune signatures track with progression of clinical disease. scRNA-seq studies performed on pulmonary tissues of patients with severe COVID-19 disease have revealed an expansion of IMs and Ficolin-1+ monocyte-derived macrophages at the expense of tissue-resident reparative alveolar macrophages (AMs) (Liao et al., 2020). The aforementioned study also observed signatures of IFN signaling and monocyte recruitment that likely contribute to the rapid decline in alveolar patency and promote ARDS. Although most of the clinical focus has been on pulmonary damage and mononuclear phagocyte (MNP) dysfunction therein, it is increasingly clear that COVID-19 likely presents systemic challenges in other organ sites, such as the ileum and kidneys. Understanding the role of non-pulmonary myeloid cells in tissue-specific pathology associated with COVID-19 will be 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