Figure 2. GA therapy changes the phenotype of human B cells in patients with MS.

Human peripheral blood mononuclear cells (PBMCs) were isolated from glatiramer acetate (GA; n = 20) or non-GA (control; n = 18) treated patients with MS. In addition, 6 patients were analyzed longitudinally on GA treatment. Red circles represent GA treatment, squares control treatment. (A) Mean frequency ± SEM of B-cell subpopulations defined as follows: transitional B cells (CD24^high CD38^high; transitional), mature B cells (CD24^var CD38^low; mature), antigen-activated B cells (CD27⁺; ag-activated), memory B cells (CD27^var CD38⁻; memory), and plasmablasts (CD20⁻ CD27⁺ CD38⁺; *p < 0.05; unpaired t test). (B) B-cell subset frequencies of patients with MS at 2 time points during GA therapy; line connects an individual patient (n = 6; *p < 0.05; Wilcoxon matched-pairs signed-rank test). (C) The individual patients' frequencies of BC subsets were correlated with the duration of GA treatment (*p < 0.05; linear regression). (D) MFI ± SEM of activation molecules expressed on B cells (ns; unpaired t test). (E) B-cell activation marker expression of patients with MS at 2 time points during GA therapy; line connects an individual patient (n = 6; *p < 0.05; Wilcoxon matched-pairs signed-rank test). (F) Mean MFI of molecules involved in antigen presentation expressed on B cells (*p < 0.05; unpaired t test). (G) Expression of molecules involved in antigen presentation of patients with MS at 2 time points during GA medication; line connects an individual patient (ns; Wilcoxon matched-pairs signed-rank test). (H) Shown is the frequency of positive cells regarding the respective cytokine (tumor necrosis factor [TNF], interleukin [IL]-6, and IL-10; mean ± SEM; ns; unpaired t test). (I) TNF, IL-6, and IL-10-positive B cells of patients with MS at 2 time points during GA medication; line connects an individual patient (*p < 0.05; Wilcoxon matched-pairs signed-rank test). GA = glatiramer acetate.