Figure 2

Anti-IL-6 treatment ameliorates clinical disease. GFAPγR1Δ and WT mice were separated into two groups with identical clinical scores at the peak of EAE and received either the isotype control α-β-gal or α-IL-6 mAb treatment. (A) Disease progression was inhibited in GFAPγR1Δ mice and recovery was promoted in WT mice by anti-IL-6 treatment. Arrowheads represent time of injection. (B) Minimal mortality in WT mice treated with α-β-gal or α-IL-6 mAb. Survival decreased in GFAPγR1Δ mice treated with isotype control mAb. By contrast, mortality was reduced by treatment of GFAPγR1Δ mice with α-IL-6 mAb. Kaplan-Meier survival curves with *P < 0.05, ***P < 0.001, log-rank test. (C, D) At day 32 post immunization (12 days after initial α-IL-6 treatment), both GFAPγR1Δ (C) and WT (D) mice treated with α-IL-6 exhibited improved clinical disease. Statistical differences determined by a two-tailed unpaired t test. Data represent the average ± SEM with GFAPγR1Δ + α-β-gal (n = 33), GFAPγR1Δ + α-IL-6 (n = 30), WT+ α-β-gal (n = 20), and WT+ α-IL-6 (n = 20) from at least three separate experiments.