Figure 5.
Anti-IL-17A therapy did not prevent the development of CsA-induced SGVHD. C3H/HeN mice were lethally irradiated (900cGy) and reconstituted with 5 × 106 ATBM from syngeneic aged-matched mice and treated for 21 days with 15mg/kg CsA. Control BMT or CsA-treated mice were then injected with 200μg of anti- IL-17 or control antibody for 7 days beginning 21 days post-BMT then every other day for 1 week. Mice were weighed individually 3 times a week and observed for symptoms of SGVHD (weight loss, diarrhea or mortality). (A) Induction of SGVHD was significantly different between BMT controls and and CsA-treated groups as determined by the log rank test (p≤0.05). (B) Percentage weight change from start of antibody treatment. Representative of 2 experiments. # p≤0.05, Control BMT (n=14) vs CsA (n=10); ## p≤0.05, Control BMT vs CsA, Control BMT anti-IL17 (n=6) vs CsA anti-IL-17A (n=8); ### p≤0.05, Control BMT vs CsA, Control anti-IL-17A vs CsA anti-IL-17A, Control Ig (n=6) vs CsA IgG (n=8). CsA vs CsA anti-IL-17A, p>0.05 at all time points. (C) In vivo anti-IL-17A therapy after CsA therapy neutralized serum levels of IL-17. Mice were induced for the development of SGVHD as described. Beginning on the last day of CsA therapy, mice were treated with 200μg/injection of anti-IL-17A mAb or control rat IgG for 7 consecutive days then every other day for an additional week. The mice were bled and the prepared serum analyzed for IL-17 by ELISA. Pooled data from 2 experiments. n = number of samples analyzed within each group.