Fig. 1
In vivo effects of cladribine on EAE score. A Oral treatment with cladribine (for 5 consecutive days—day 5 to 9, as indicated in the figure) induced a less severe disease course in EAE mice compared to EAE mice receiving vehicle. Statistical differences were observed in terms of development of neurological signs over the whole observation period until day 27 (two-way ANOVA, F (1, 22) = 9.446, p = 0.0056, n = 12 for each group). B The bar graph depicts the cumulative EAE score of both experimental groups on the day of maximal clinical deterioration (dmax, unpaired Mann–Whitney U test, U = 34.50, p = 0.0295, n = 12 for each group). C Immunophenotypings of the peripheral blood (a), LNs (b), spleen (c), thymus (d) and bone marrow (e) at dmax were performed by flow cytometry. Immune cell profiles of mice treated with cladribine were compared to those receiving vehicle. Statistically significant differences were obtained by performing two-way ANOVAs complemented by Bonferroni test for multiple comparisons, n = 3 for each group. p-values: 0.0019 (a, blood), 0.0003 (b, LN), 0.6227 (c, spleen), 0.0016 (d, thymus) and 0.3734 (e, bone marrow). D Flow cytometric analyses were used, to evaluate the immune cell distribution in the brain (a) and spinal cord (b) of EAE mice, either treated with cladribine or vehicle at dmax. Statistically significant differences were obtained by performing two-way ANOVAs complemented by Bonferroni test for multiple comparisons, n = 3 for each group. p-value was 0.2486 for brain, < 0.0001 for spinal cord. p > 0.05 = ns, p < 0.05 = *, p < 0.01 = **, p < 0.001 = ***, p < 0.0001 = ****