Figure 6
Figure 6. Regulatory effect of peripheral blood B cells. Monocytes were purified from the peripheral blood of (A) healthy donors, (B) patients with SLE, or (C) patients with RA and stimulated with GM-CSF (1000 U/mL) and IL-4 (500 U/mL) for 6 days. The differentiated immature DCs were stimulated with LPS (100 ng/mL) and IFN-γ (1000 U/mL) for 24 hours to generate mature DCs. Peripheral blood B cells were stimulated for 5 days on CD40L-transfected NIH-3T3 murine fibroblasts in the presence of 0.25μM CpG-ODN 2006. (A) B cells from healthy donors were added to their autologous DCs (ratio 1 DC/4 B cells) either nonstimulated (NS) or stimulated (S) with their supernatant. MFI of HLA-DR (7 samples), percentages of CD80low (8 samples), CD86low (8 samples), and IL-12low (7 samples) DCs were evaluated by flow cytometry on CD19-negative cells. (B) B cells from patients with SLE or (C) from patients with RA were activated as described previously and added with their supernatant to autologous DCs. MFI of HLA-DR (6 and 8 samples for SLE and RA patients, respectively), percentages of CD80low (8 and 10 samples for SLE and RA patients, respectively), CD86low (6 and 10 samples for SLE and RA patients, respectively), and IL-12low (7 and 10 samples for SLE and RA patients, respectively) DCs were evaluated by flow cytometry on CD19-negative cells. Activated tonsillar B cells were used as controls (Ctrl). *P < .05; **P < .01; ns, nonsignificant.

Regulatory effect of peripheral blood B cells. Monocytes were purified from the peripheral blood of (A) healthy donors, (B) patients with SLE, or (C) patients with RA and stimulated with GM-CSF (1000 U/mL) and IL-4 (500 U/mL) for 6 days. The differentiated immature DCs were stimulated with LPS (100 ng/mL) and IFN-γ (1000 U/mL) for 24 hours to generate mature DCs. Peripheral blood B cells were stimulated for 5 days on CD40L-transfected NIH-3T3 murine fibroblasts in the presence of 0.25μM CpG-ODN 2006. (A) B cells from healthy donors were added to their autologous DCs (ratio 1 DC/4 B cells) either nonstimulated (NS) or stimulated (S) with their supernatant. MFI of HLA-DR (7 samples), percentages of CD80low (8 samples), CD86low (8 samples), and IL-12low (7 samples) DCs were evaluated by flow cytometry on CD19-negative cells. (B) B cells from patients with SLE or (C) from patients with RA were activated as described previously and added with their supernatant to autologous DCs. MFI of HLA-DR (6 and 8 samples for SLE and RA patients, respectively), percentages of CD80low (8 and 10 samples for SLE and RA patients, respectively), CD86low (6 and 10 samples for SLE and RA patients, respectively), and IL-12low (7 and 10 samples for SLE and RA patients, respectively) DCs were evaluated by flow cytometry on CD19-negative cells. Activated tonsillar B cells were used as controls (Ctrl). *P < .05; **P < .01; ns, nonsignificant.

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