Figure 2
Figure 2. Neutrophil depletion attenuates established CIA. (A) Clinical scores (mean ± SEM) in WT DBA/1 mice treated with either isotype control mAb or anti–Gr-1 mAb after the onset of CIA. P < .001 during days 1 to 14 of arthritis. (B) Incidence of disease (percentage of total mice) in isotype control and anti–Gr-1 mAb-treated mice during 14 days of treatment. P < .001 at day 14. In panels A and B, n = 22 to 23 mice per treatment group; data pooled from 3 independent experiments. Histologic sections of typical joints from (C) anti–Gr-1 mAb and (D) isotype control mAb-treated mice. E indicates exudate; JS, joint space; C, cartilage; B, bone; and S, synovium. Magnification, ×200 (H&E stained). (E) Clinical scores (mean ± SEM) in WT DBA/1 mice treated with either isotype control mAb or anti-Ly6G mAb (1A8) after the onset of CIA. n = 8 mice per treatment group. P < .01 during days 1 to 14 of arthritis.

Neutrophil depletion attenuates established CIA. (A) Clinical scores (mean ± SEM) in WT DBA/1 mice treated with either isotype control mAb or anti–Gr-1 mAb after the onset of CIA. P < .001 during days 1 to 14 of arthritis. (B) Incidence of disease (percentage of total mice) in isotype control and anti–Gr-1 mAb-treated mice during 14 days of treatment. P < .001 at day 14. In panels A and B, n = 22 to 23 mice per treatment group; data pooled from 3 independent experiments. Histologic sections of typical joints from (C) anti–Gr-1 mAb and (D) isotype control mAb-treated mice. E indicates exudate; JS, joint space; C, cartilage; B, bone; and S, synovium. Magnification, ×200 (H&E stained). (E) Clinical scores (mean ± SEM) in WT DBA/1 mice treated with either isotype control mAb or anti-Ly6G mAb (1A8) after the onset of CIA. n = 8 mice per treatment group. P < .01 during days 1 to 14 of arthritis.

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