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. 2019 May 30;177(6):1566–1582.e17. doi: 10.1016/j.cell.2019.04.036

Figure 3.

Figure 3

Evidence for Prolonged B Cell Activation following EBOV Infection

(A) Frequency of GP-specific memory B cells over time. The percentage GPcl binding cells is shown.

(B and C) Prolonged activation of EBOV-specific MBCs. The percentage of cells expressing the activation marker CD71 is shown for GPcl binding MBCs (B) or total MBCs (C).

(D) Affinity maturation of GP-specific IgG. The avidity index is the percentage of GP-specific antibody (measured by ELISA) able to remain bound after washing with 8 M urea. The mean and standard deviation of three assays is shown.

(E) Longitudinal CXCL13 levels in serum. Plasma levels of the germinal center-associated chemokine CXCL13 were determined using a commercial assay. The normal reference range is shaded gray and the limit of detection is indicated by the dotted line. Sample taken shortly after uveitis episode.

(F) Increase in SHM over time in GP-specific mAbs. Bars show the median SHM% and interquartile ranges. The p value for the Wilcoxon rank-sum test is shown.

(G and H) SHM% of GP-binding IGH lineages from repertoire sequencing. Unpaired analysis of all lineages that included sequences from GP-binding cells is shown in (G). Paired analysis of GP-binding lineages detectable at multiple time points is shown in (H). Bars show the median SHM% and interquartile ranges. p values are for the Wilcoxon rank-sum test (G) or the Wilcoxon signed-rank test (H). EVD9 day 40 sequences were derived from sorted ASC RNA.

See also Figure S3 and Table S1.