Fig. 1

Hypercholesterolemia induced by LDLr deficiency do not exacerbate EAE disease. A Serum level of total cholesterol (tChol) in female LDLr^−/− (mean ± SD; n = 6) and wild-type mice (mean ± SD; n = 12 mice). B EAE in female wild-type and LDLr^−/− mice. The course of EAE is shown as clinical score (mean ± SEM; n = 8 mice). C EAE in male wild-type and LDLr^−/− mice. The course of EAE is shown as clinical score (mean ± SEM; n = 9 mice). The female and male EAE experiments were not performed at the same time. Data are representative of three experiments. D Histopathological stainings and quantifications of spinal cord sections of non-immunized WT (WT NI) or immunized WT and LDLr^−/− mice at day 16 post-immunization for cellular infiltration (H&E). Five sections per mouse were quantified (n = 3 mice). Scale bars 500 µm (top panels), 100 µm (bottom panels). E Flow cytometry analysis of the total proportion (%) of the leukocyte (viable CD45⁺), lymphocyte T (CD3⁺) and lymphocyte T CD4⁺ (CD4⁺) in the CNS 14 days after EAE immunization (mean ± SD; n = 3–5 mice). ∗∗∗∗p < 0.0001; NS, not significant; p values were determined by unpaired Student’s t test (A and D), a Mann–Whitney U test (B, C) and a two-way ANOVA with Sidak’s post hoc test (E).