Figure 5

Treating mice with the AA98 antibody reduces both the severity of EAE and the infiltration of lymphocytes into the CNS.

(a) Mice treated with either the AA98 antibody or the control mIgG have a similar time of onset and incidence of EAE following immunization. (b and c) Mice that received preventive treatment with the AA98 antibody had lower mean clinical scores and less EAE severity (defined as a clinical score ≥3) than control-treated mice (n = 11 mice/group). (d) Luxol fast blue staining of spinal cord sections from control mIgG-treated and AA98-treated mice with EAE (n = 5 mice/group, 15 lesions/mouse). Scale bar, 200 μm. (e) Flow cytometry analysis of the number and percentage of infiltrated leukocytes (CD45^highCD11b⁻) isolated from the CNS of mIgG-treated and AA98-treated mice (n = 5 mice/group). (f) Flow cytometry analysis of the proportion of CD4⁺ and CD8⁺ cell (in CD45^highCD11b⁻ cells), T_H1 and T_H17 cells (in CD4⁺ T cells) and CD146⁺ T lymphocytes from mIgG-treated and AA98-treated mice (n = 5 mice/group). (g–j) Mean clinical scores (g and h) and percentage of mice with severe EAE (clinical score ≥3) (i and j) for mIgG-treated and AA98-treated mice with active EAE (g and i; n = 7 mice/group) or passive EAE (h and j; n = 5 mice/group). The arrows in panels g and h indicate the onset of remission, reflected by a significant decrease in the mean clinical score. (k) Luxol fast blue staining and analysis of the demyelinating lesions and area in mIgG-treated and AA98-treated mice with EAE (n = 7 mice/group). Scale bar, 200 μm. (l and m) Flow cytometry analysis of CD45^high+CD11b⁻ cells (l) as well as CD4⁺ and CD8⁺ cell (in CD45^highCD11b⁻ cells), T_H1 and T_H17 cells (in CD4⁺ T cells) and CD146⁺ T cells (m) in mIgG-treated and AA98-treated mice with EAE (n = 5 mice/group). *, p < 0.05; **, p < 0.01, ***, p < 0.001.