Figure 4.

Prevention of spontaneous autoimmune polyneuropathy (SAP) by adoptive transfer (AT) of wild‐type regulatory B cells (B_reg) into asymptomatic B7‐2^–/– non‐obese diabetic (NOD) mice. (a) Clinical severity. B_regs (CD19⁺CD1d^hiCD5⁺) and non‐B_regs (CD19⁺CD1d^–CD5^–) were sorted from splenocytes and lymph node (LN) cells of 2‐month‐old WT NOD mice at day 20 post‐immunization with P0 (200 μg), and 1 × 10⁶ sorted cells were injected via tail vein into 5‐month‐old female B7‐2^–/– NOD mice. Comparing B_reg (AT) versus non‐B_reg (AT) or phosphate‐buffered saline (PBS) (no AT), *P < 0·0005 (n = 6–8) for clinical scores (left panel), grip strength measurements (middle panel) and all the parameters of sciatic motor responses. (b) Splenocyte proliferation, B10 cells and regulatory T cells (T_regs) at 12 weeks post‐AT. Left panel: splenocyte proliferation based on [³H]‐thymidine incorporation. [Ag]: 20 μg/ml; treatment duration: 72 h. *P < 0·0002 (n = 6–8). Middle panel: B10 cells. *P < 0·0002 for splenic B10 cells; #P < 0·03 for LN B10 cells (n = 6). Right panel: T_regs. *P < 0·0002 for splenic T_regs, #P < 0·03 for LN T_reg cells (n = 6). (c) T cell cytokine profile at 12 weeks post‐AT. *P < 0·0001 (n = 6) for spleen and LN CD4⁺IL‐10⁺ cells.