Fig. 4.

Treatment with anti-GM-CSF antibody at either induction or effector phase of EAU suppresses disease in Ifng^−/−Il17a^−/− mice. WT and Ifng^−/−Il17a^−/− mice either on C57BL/6 (immunized with IRBP and p1–20) (B, D, E) or on B10.RIII background (immunized with p161–180) (G, H) were i.p. treated with anti-GMCSF mAb (MP1–22E9.11) or isotype Ig (Rat IgG2a) from the induction phase (starting on day −1) (A, B, G) or from the effector phase (starting on day 7) (C, D, H) of EAU induction every other day. (E) T cells were enriched from LNs and spleens of EAU-induced WT and Ifng^−/−Il17a^−/− mice, were restimulated in vitro with IRBP for 3 days and were adoptively transferred to naïve recipient mice that received treatment of 300 μg of anti-GM-CSF mAb or isotype control every other day starting from the day of cell transfer. (F) WT and Ifng^−/−Il17a^−/− mice were immunized for EAU. On day 10, 100 μg of anti-GM-CSF mAb in 2 μl of PBS was intravitreally injected into the right eye and the isotype control was injected into the left eye of each mouse. EAU scores were assessed by histology on day 12. Representative data from 2 (E, F) or 3 (B, D, G, H) independent experiments, and each group contains at least 3 mice. Data shown as mean ± SEM. *p < 0.05, ****p < 0.0001, (B, D, E, G, H) Mann-Whitney U test, (F) Wilcoxon matched-pairs signed rank test. NS, not significant.