PMC:7402624 / 29832-31625 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":"During acute viral infections or vaccination, PB responses are transiently detectable in the blood and correlate with cTfh responses (40). Comparing the frequency of PB to the frequency of total cTfh or activated cTfh, however, revealed a weak correlation only with activated cTfh (Fig. 4F and fig. S5, B and C). Furthermore, some patients had robust activated cTfh responses but PB frequencies similar to controls, whereas other patients with robust PB responses had relatively low frequencies of activated cTfh (Fig. 4F and fig. S5, B and C). However, there was also an association between PB frequency and CD38+HLA-DR+ or KI67+ CD4 T cells that might reflect a role for non-CXCR5+ CD4 T cell help (fig. S5D), but such a relationship did not exist for the equivalent CD8 T cell populations (fig. S5E). Although ~70% of COVID-19 patients analyzed made antibodies against SARS-CoV2 spike protein (79/111 IgG; 77/115 IgM (44)), antibody levels did not correlate with PB frequencies (Fig. 4G and fig. S5F). The occasional lack of antibody did not appear to be related to immunosuppression in a small number of patients (fig. S5G). The lack of PB correlation with antibody suggests that a proportion of these large PB responses were: i) generated against SARS-CoV2 antigens other than the spike protein or ii) inflammation-driven and perhaps non-specific or low affinity. Notably, anti-SARS-CoV2 IgG and IgM levels correlated with the activated, but not total, cTfh response, suggesting that at least a proportion of cTfh were providing SARS-CoV2-specific help to B cells (Fig. 4, H and I, and fig. S5, H and I). Although defining the precise specificity of the robust PB populations will require future studies, these data suggest that at least some of the PB response is specific for 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