PMC:7402624 / 24155-26371 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7402624","sourcedb":"PMC","sourceid":"7402624","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7402624","text":"A key feature of COVID-19 disease is thought to be an inflammatory response that, at least in some patients, is linked to clinical disease manifestation (2, 4) and high levels of chemokines/cytokines, including IL-1RA, IL-6, IL-8, IL-10, and CXCL10 (11, 41). To investigate the potential connection of inflammatory pathways to T cell responses, we performed 31-plex Luminex analysis on paired plasma and culture supernatants of anti-CD3/anti-CD28 stimulated PBMC from a subset of COVID-19 patients and HD controls. Due to biosafety restrictions, only eight COVID-19 patient blood samples that were confirmed SARS-CoV2 RNA negative in the blood by PCR could be studied (fig. S4A). Half of these COVID-19 patients had plasma CXCL10 concentrations that were ~15 fold higher than HD controls, whereas the remainder showed only a limited increase (fig. S4B). CXCL9, CCL2, and IL-1RA were also significantly increased. In contrast, chemokines involved in the recruitment of eosinophils (eotaxin) or activated T cells (CCL5) were decreased. IL-6 was not elevated in this group of patients, in contrast to the subset of individuals tested clinically (fig. S1B), potentially because IL-6 was measured in the hospital setting often when systemic inflammation was suspected. Following stimulation in vitro, PBMC from COVID-19 patients produced more CCL2, CXCL10, eotaxin, and IL-1RA than HD (fig. S4, C and D) and concentrations of CXCL10 and CCL2 correlated between the matched supernatant from stimulated PBMC and plasma samples (fig. S4E). Finally, we investigated whether CD8 T cells from COVID-19 subjects were capable of producing IFNɣ following polyclonal stimulation. Following ɑCD3+ɑCD28 stimulation, similar proportions of CD8 T cells from COVID-19 patients and HD controls produced IFNɣ, suggesting that PBMC from COVID-19 patients were responsive to TCR crosslinking (fig. S4, F to H). The ability of T cells to produce IFNɣ following stimulation occurred in patients with increases in KI67 as well as patients with low KI67 (fig. S4, F to H). Taken together, these data support the notion that a subgroup of COVID-19 patients has elevated systemic cytokines and chemokines, including myeloid recruiting 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