Figure 4.
CD70+CD39+EBNA2+B cells accumulate upon loss of CD27-mediated immune control of EBV. (A) Frequency of CD70 expression on CD19+ B cells in multiple organs (blood, spleen, and liver) in anti-CD27 blocking antibody– vs isotype control antibody–treated group. (B) Flow cytometry plots of CD39 and CD73 expression on CD19+ B cells in multiple organs (blood, spleen, and liver) in the indicated experimental groups. (C) Frequency of CD39 expression on CD19+ B cells. (D) Correlation between the CD39 expression on CD19+ B cells and EBV viral loads in blood. (E) Frequency of CXCR5 expression on CD19+ B cells. (F) Representative uniform manifold approximation and projection (UMAP) analysis depicts clusters with coexpression of CD39, CD70, Ki67, and EBNA2 on CD19+ B cells in blood. (G) Data from panel F were transformed and shown in percentile of each population in anti-CD27 blocking antibody– vs isotype control antibody–treated group. (H) Representative heatmap analysis of coexpression of CD39, CD70, Ki67 and EBNA2 on CD19+ B cells in blood. Data (n = 14-16 per group) pooled from 2 independent mouse experiments were graphed (A,C-E) and displayed with median and interquartile range. Graphs (F-H) (n = 7-8 per group) are representative from 1 of 2 independent experiments. The Mann-Whitney U test was used to assess P values (A,C,E), and the Spearman correlation examining rank correlation was used for panel D. *P < .05, **P < .01, ***P < .001. See also related supplemental Figure 4.