PMC:7402624 / 27173-28450 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":"I67 expression was markedly elevated in all B cell subpopulations in COVID-19 patients compared to either control group (Fig. 4C). This observation suggests a role for an antigen-driven response to infection and/or lymphopenia-driven proliferation. Higher KI67 in PB may reflect recent generation in the COVID-19 patients compared to HD or RD. CXCR5 expression was also reduced on all major B cell subsets in COVID-19 patients (Fig. 4D). Loss of CXCR5 was not specific to B cells, however, as expression was also decreased on non-naïve CD4 T cells (Fig. 4E). Changes in the B cell subsets were not associated with co-infection, immune suppression, or treatment with steroids or other clinical features, though a possible negative association of IL-6 and PB was revealed (fig. S5A). These observations suggest that the B cell response phenotype of COVID-19 disease was not simply due to systemic inflammation.\nFig. 4 Deep profiling of COVID-19 patient B cell populations reveals robust plasmablast populations and other B cell alterations.\n(A) Gating strategy and frequencies of non-PB B cell subsets. (B) Representative flow cytometry plots and frequencies of PB; green line at upper decile of HD. (C) Representative flow cytometry plots and frequencies of KI67+ B cells. 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