Anti–IL-23 therapy inhibits multiple inflammatory pathways and ameliorates autoimmune encephalomyelitis
J. Clin. Invest. Yi Chen, et al. 116:1317 doi:10.1172/JCI25308 [Go to this article.]

Figure 5
Anti–IL-23 therapy inhibits PLP epitope spreading and relapsing EAE. (A) Average clinical score of mice treated with anti–IL-23p19 (clone MB490) or anti-p40 antibody on the day of EAE onset. The first antibody dose was given by the i.v. route at the first sign of clinical disease and the 2 subsequent doses by the s.c. route at days 7 and 14 after EAE onset. One of 3 experiments is shown. Disease relapse incidence and histopathology scores are shown in Table 3. Arrows indicate the day of initial mAb treatment (day of disease onset). (B) Epitope spreading was determined by analysis of DLN cells or purified CNS mononuclear cells for response to PLP_139–151 or PLP_178–191 on either the day of disease onset or during disease relapse. Purified CNS mononuclear cells from mice treated with anti–IL-23p19 or isotype control mAbs were stimulated for 4 days with PLP peptides then pulsed with ³[H] 16 hours before proliferation assay. Cells from 3 to 4 mice of each treatment group were pooled and cultured at indicated PLP peptide concentration in triplicate wells. Results from 1 of 2 experiments are shown.