Id |
Subject |
Object |
Predicate |
Lexical cue |
T159 |
0-60 |
Sentence |
denotes |
B cell subpopulations were also altered in COVID-19 disease. |
T160 |
61-275 |
Sentence |
denotes |
Whereas naïve B cell frequencies were similar in COVID-19 patients and RD or HD, the frequencies of class-switched (IgD−CD27+) and not-class-switched (IgD+CD27+) memory B cells were significantly reduced (Fig. 4A). |
T161 |
276-387 |
Sentence |
denotes |
Conversely, frequencies of CD27−IgD− B cells and CD27+CD38+ PB were often robustly increased (Fig. 4, A and B). |
T162 |
388-525 |
Sentence |
denotes |
In some cases, PB represented >30% of circulating B cells, similar to levels observed in acute Ebola or Dengue virus infections (42, 43). |
T163 |
526-679 |
Sentence |
denotes |
However, these PB responses were only observed in ~2/3 of patients, with the remaining patients displaying PB frequencies similar to HD and RD (Fig. 4B). |
T164 |
680-811 |
Sentence |
denotes |
KI67 expression was markedly elevated in all B cell subpopulations in COVID-19 patients compared to either control group (Fig. 4C). |
T165 |
812-929 |
Sentence |
denotes |
This observation suggests a role for an antigen-driven response to infection and/or lymphopenia-driven proliferation. |
T166 |
930-1024 |
Sentence |
denotes |
Higher KI67 in PB may reflect recent generation in the COVID-19 patients compared to HD or RD. |
T167 |
1025-1118 |
Sentence |
denotes |
CXCR5 expression was also reduced on all major B cell subsets in COVID-19 patients (Fig. 4D). |
T168 |
1119-1239 |
Sentence |
denotes |
Loss of CXCR5 was not specific to B cells, however, as expression was also decreased on non-naïve CD4 T cells (Fig. 4E). |
T169 |
1240-1462 |
Sentence |
denotes |
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). |
T170 |
1463-1589 |
Sentence |
denotes |
These observations suggest that the B cell response phenotype of COVID-19 disease was not simply due to systemic inflammation. |