PMC:7200337 / 90125-91400 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":"Several studies have begun to report the cellular programs that may contribute to the cytokine storm detected in COVID-19 patients. One group reported that in the context of generalized lymphopenia, certain subsets of CD4 T cells that express GM-CSF and IL-6 are more abundant in severe COVID-19 patients than in COVID-19 patients who do not require intensive care (Zhou et al., 2020b). Reports that other major proinflammatory cytokines (TNF-α, IFN-ɣ, IL-2) and chemokines (CCL2, CCL3, CCL4) are elevated underscore a potentially pathogenic TH1/2 program in COVID-19 (Diao et al., 2020, Giamarellos-Bourboulis et al., 2020). Histological and single-cell analyses identified monocytes and macrophages as other potent sources of inflammatory cytokines in COVID-19 cytokine storm (Chen et al., 2020h, Giamarellos-Bourboulis et al., 2020, Law et al., 2005, Moore and June, 2020, Zhou et al., 2020b). Studies of other betacoronavirus infections, including SARS-CoV-1 and MERS-CoV, have also identified similar hyperactivation of monocytes, macrophages, and DCs as a driver of cytokine-mediated immunopathology in humans (Cheung et al., 2005, Chien et al., 2006, Huang et al., 2020c, Konig et al., 2020, Wang et al., 2005, Wong et al., 2004, Xu et al., 2020b, Zhou et al., 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