Figure 2
Effect of glatiramer acetate on [Ca2+]i homeostasis. (A) Confocal immunofluorescence images depicting FITC-CD19+ B cells in PBMCs isolated from naïve (a) or glatiramer acetate (GA) (b) patients. Panel c shows the brightfield image of panel b; d, higher magnification of the frame in c showing a single FITC-CD19+ cell. Arrows point to FITC-CD19+ cells, arrowheads point to FITC-CD19− cells. (B) Quantification of ex vivo microfluorimetric experiments showing the effect of ATP+ thapsigargin on [Ca2+]i in PBMCs from healthy subjects (Ctl) (N = 80 cells), from patients treated with GA (N = 40 cells), interferon (INF) β-1b (N = 40 cells), INFβ-1a (N = 40 cells), and from drugs-naïve patients (N = 50 cells). *p < 0.05 vs all. (C) Representative traces of the effects of ATP+ thapsigargin on [Ca2+]i in FITC-CD19+ and FITC-CD19− cells of PBMCs isolated from GA treated patients. (D) Quantification of the effects of ATP+ thapsigargin on [Ca2+]i in FITC-CD19+ and FITC-CD19− cells from GA treated patients and healthy subjects. *p < 0.05 vs all. (E) Quantification of the effects of ATP+ thapsigargin on [Ca2+]i in FITC-CD19+ cells obtained from drugs naïve RR-MS patients treated or not in vitro with GA. *p < 0.05 vs drug-naïve RR-MS. Data are expressed as mean ± S.E.M of three independent experiments for each condition. Statistical analysis was performed using the one-way ANOVA or t-test followed by Newman Keul’s test. p < 0.05 was considered statistically significant.
