Fig. 5

CXCR3 KO ameliorates BBB pathology. a-c Quantitative RT-PCR analysis on dissected corpus callosum tissue samples from wild type (red) or CXCR3 deficient (blue) mice after 5 days cuprizone administration or untreated control mice. Results are expressed as mean fold change of N = 3–4 mice ± s.e.m., normalized to untreated wild type control animals (set to 1; gray line, N = 5). Assessed were (a) cellular markers, (b) cytokines and chemokines, and (c) endothelial and BBB promoting markers as indicated. Significance between WT mice and CXCR3 mice was evaluated by Student’s t-test for each individual gene (*P < 0.05, **P < 0.01, ***P < 0.001). d-f Brain water (d, g/g dry brain), of extravasated EB (e), and NaFl (f) in untreated wild type controls (white, N = 3–4), and wild type (red, N = 3–4) or CXCR3 deficient (blue, N = 3) mice exposed to cuprizone for 5 days. Significance to control was evaluated by 1way ANOVA with Tukey’s post test (*P < 0.05, **P < 0.01, ***P < 0.001). g Quantitative RT-PCR on isolated cells as indicated from brain of from WT or CXCR3 deficient mice after 5 days cuprizone administration or untreated control mice. Results show fold-change values according to color code of individual animals (N = 3) normalized to the mean of untreated control animals (set to 1; N = 5)