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. 2016 Aug 18;113(35):9816–9821. doi: 10.1073/pnas.1611189113

Fig. 4.

Fig. 4.

CLCa-null B cells have increased CXCR4 surface levels and impaired ligand-induced CXCR4 internalization. (A) Ratios of the mean fluorescence intensity (MFI) of CXCR4 and B220 on WT or CLCa-null (KO) donor cells (CD45.2+) to MFIs on C57BL/6 (B6) (CD45.1+CD45.2+) donor cells for germinal center (GC) B cells from lymphoid tissues indicated from WT/B6 and KO/B6 chimeras (mean ± SEM; n = 42 for Peyer’s patches, n > 11 for spleen, from at least three pairs of different donors for mixed chimera mice, **P < 0.01, ***P < 0.001; P values, unpaired t test). (B) MFI ratios for CXCR5 and B220 on WT or KO donor follicular (Fo B) or GC B cells (CD45.2+) relative to B6 donor B-cell populations (CD45.1+CD45.2+) from mesenteric lymph nodes (mLNs) (mean ± SEM; n > 11). (C) Percent CXCR4 internalized at 37 °C over time after addition of SDF1 (relative to surface CXCR4 on control cells similarly treated with PBS) for Fo B and GC B cells from mLNs of WT or KO mice (mean ± SEM of n = 5 WT and n = 6 KO from two independent experiments, *P < 0.05; P values, two-way ANOVA with Bonferroni post tests). (D) Percent CXCR5 internalized at 37 °C over time after addition of CXCL13 (relative to surface CXCR5 on control cells similarly treated with PBS) for Fo B and GC B cells from mLNs of WT or KO mice (mean ± SEM of n = 5 WT and n = 5 KO mice, from two independent experiments).