Fig. 6. Combined treatment using anti–VCAM-1 and anti–ICAM-1 antibodies ameliorates symptoms of pericyte-deficient and control mice after the induction of EAE. (A) Scoring of clinical symptoms during the course of anti–VCAM-1 and anti–ICAM-1 mAb treatment after induction of active EAE of control mice. (B) Kaplan–Meier survival curves of isotype control and anti–VCAM-1 and anti–ICAM-1 monoclonal antibody (α-VCAM-1 and α-ICAM-1 mAb) treated Pdgfbret/ret mice after active induction of EAE (P = 0.05, log-rank test). (C) Scoring of clinical symptoms during the course of anti–VCAM-1 and anti–ICAM-1 mAb treatment after induction of active EAE in Pdgfbret/ret mice (C). (A–C) The EAE or ataxia score of each mouse is plotted. Arrowheads indicate when mice reached termination criteria and were euthanized for analysis. The experiment was terminated on day 20 (black dashed line; n = 4 mice treated with isotype control, n = 4 mice treated with anti–VCAM-1 and anti–ICAM-1 mAb). (D and E) Quantification of the absolute cell numbers of different immune cell populations (gating shown in SI Appendix, Fig. S12) in the brains (D) and spinal cords (E) of isotype control and anti–VCAM-1 and anti–ICAM-1 mAb-treated control and Pdgfbret/ret mice using flow cytometry. Controls, n = 4 mice per group; Pdgfbret/ret mice, n = 3 mice per group. Pooled data from two independent experiments. Data are presented as the mean ± SD. Two-way ANOVA followed by Šídák’s post hoc test was used to determine statistical significance between groups.
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