Figure 2.

Treatment with CD52 antibody improves symptoms and pathological changes of C57BL/6J EAE mice. EAE mice established by vaccinating C57BL/6J mice with MOG35-55 were treated with CD52 antibodies or PBS at the peak of disease (~ 16 dpi). Treatments with anti-CD52 significantly attenuated clinical scores of EAE mice [(A) two-way ANOVA, F (1, 11) = 33.07; n ≥ 5 per group], and increased the body weight, although it was not statistically significant [(B) two-way ANOVA, F (1, 11) = 2.392; n ≥ 5 per group]. Two weeks after treatments, EAE mice were analyzed for axonal degeneration and myelin loss. Treatments with CD52 antibodies significantly reduced APP-positive spheroids (in brown) [(C, D) t test, t (7) = 4.485; n ≥ 4 per group], and markedly increased the coverage of MOG-positive myelin (in green) [(E, F) t test, t (11) = 2.978; n ≥ 5 per group] in the white matter of anterior and lateral columns at the lumber spinal cord (as shown in E with the frame), compared with PBS-treated EAE mice. The presented images are from EAE mice 14 days post treatments. Interestingly, the number of APP-positive spheroids was negatively correlated with the area of MOG-positive myelin [(G) Pearson correlation test; n = 9]. EAE mice were also analyzed within 4 days after treatments. Anti-CD52 treatment immediately reduced the clinical scores of EAE mice [(H) two-way ANOVA, F (1, 15) = 17.24; n ≥ 8 per group], and increased the body weight, although not statistically significant [(I) two-way ANOVA, F (1, 15) = 1.515; n ≥ 8 per group]. Histological analysis showed that treatments with anti-CD52 antibodies significantly decreased the number of APP-positive spheroids [(J) t test, t (12) = 2.339; n = 7 per group] but did not change the coverage of MOG-positive myelin in the white matter of lumber spinal cord [(K) t test, t (16) = 1.581; n ≥ 8 per group].