Anti-Ly6G attenuates arthritis and inhibits neutrophil recruitment in joints and peritoneum. (A) Arthritic response of mice given 5 μg of Ab twice and 150 μL of K/BxN serum (rat IgG2a isotype, n = 14; anti-Ly6B.2, n = 8; anti-Ly6G, n = 12 pooled from 2-6 experiments). Shown is isotype (Iso) versus anti-Ly6G. P < .0001 by ANOVA. (B) K/BxN serum–induced flare was assessed 30 minutes after the first injection of K/BxN serum using the same scoring system as in panel A. (C) Representative sections of day-4 ankle histopathology from mice receiving isotype control Ab or anti-Ly6G (H&E stain; 20× objective). JC indicates joint cavity; and S, synovium. Right panel shows the quantification of neutrophils per 3 high-power field of day-4 ankle tissue (n = 12-18 ankles). (D) Treatment of active arthritis with nondepleting and depleting doses of anti-Ly6G. Two doses of anti-Ly6G at 5 or 50 μg/dose or control Ab at 50 μg/dose were administered intraperitoneally on days 6 and 9 of active arthritis. Circulating neutrophils were enumerated by automated cytometer on day 11. (E) Effect of anti-Ly6G (5 μg intraperitoneally on days −1 and 2) on neutrophils in the blood and BM of otherwise unmanipulated mice (n = 5-12 mice/time point from 4 experiments). There was a trend toward decreased neutrophil counts in blood 30 minutes after injection (P = .12). nd indicates not done. (F) Anti-Ly6G (5 μg) was administered intraperitoneally to nonarthritic mice and TG instilled intraperitoneally at the equivalent of day 4 of arthritis. Peritoneal cells were harvested at 4 hours by lavage and neutrophils enumerated by flow cytometry. Data are from n = 6 animals per group from 2 experiments. *P < .05; **P < .01.