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. 2019 Oct 16;134(22):1997. doi: 10.1182/blood.2019003731

Bai X, Zhang Y, Huang L, et al. The early activation of memory B cells from Wiskott-Aldrich syndrome patients is suppressed by CD19 downregulation. Blood. 2016;128(13):1723-1734.

PMCID: PMC7218721  PMID: 31778546

In Figure 3A on page 1728, the images are duplicates of those in Figure 3C due to a publisher error that occurred during the publication process. The corrected Figure 3 is shown below. The publisher apologizes for the error, which has been corrected in the online version of the article.

Figure 3.

Figure 3.

The recruitment of pCD19 was decreased in WAS memory B cells, but the recruitment of phosphorylated SHIP (pSHIP) was increased in WAS memory B cells. (A-D) TIRFM and IRM analysis of pCD19 staining in the contact zone of HCs and WAS (P1-12) memory and naive B cells incubated with membrane-tethered Fab′–anti-Ig. The colocalization coefficients between BCR and pCD19 staining were determined using NIS-Elements AR 3.2 (F). Shown are representative images (A-D) and the average MFI (E) or colocalization coefficients (F) (±SD) from ∼50 individual cells of 3 independent experiments. (G-J) TIRFM and IRM analysis of pSHIP staining in the contact zone of HCs and WAS (P1-12) naive and memory B cells incubated with membrane-tethered Fab′–anti-Ig. Shown are representative images (G-J) and the MFI (±SD) of pSHIP (K) in the B-cell contact zone from 3 independent experiments. TIRFM analysis of the spatial relationship of BCR with pSHIP (G-J) in the contact zone of B cells incubated with membrane-tethered Fab′–anti-Ig. The colocalization coefficients between BCR and pSHIP staining were determined using NIS-Elements AR 3.2 software (L). Bars, 2.5 μm. *P < .01, compared with WAS naive or memory B cells.


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