Fig. 7.

Lowering cellular cholesterol rescues the phenotype of apoE4 MDCs. a–c Median fluorescence intensity (MFI) of lipid rafts (CTXb, a), HLA-DR (b), CD80 (c) in immature (LPS−) and mature (LPS+) MDCs. d and e Relative quantification of lipid rafts (CTXb, d) and free cholesterol (filipin, e) in immature (LPS−) or mature (LPS+) apoE4 MDCs cultured with serum derived from an allogenic apoE4 donor as compared to an apoE3 donor. Data are presented as relative expression compared to immature apoE4 MDCs cultured with serum from an allogenic apoE4 donor. f Determination (ng/µg) of sterols and oxysterols by gas chromatography-mass spectrometry of mature (LPS+) apoE4 MDCs cultured with serum from an allogenic apoE4 or apoE3 donor. g Relative expression of HLA-DR in immature (LPS−) or mature (LPS+) apoE4 MDCs cultured with serum derived from an apoE4 donor as compared to immature (LPS−) apoE4 MDCs cultured with serum from an apoE4 donor; data are presented as relative expression (calculated from HLA-DR⁺ cells) compared to immature apoE4 MDCs cultured with serum from an apoE4 donor. h Differentiation of CD4⁺ T naive cells from a carrier of apoE3 isoform with allogenic mature (LPS+) apoE4 MDCs cultured with serum from an apoE4 or apoE3 donor. i Heat-map of lipid-related and inflammatory genes in mature (LPS+) MDCs from apoE4 carriers cultured in the presence of serum from allogenic apoE4 or an apoE3 donor; data are presented as relative to mean expression in apoE3 DCs (log2 scale). N = 4–6 per group. Statistical analysis was performed with two-way Anova. Data are reported as mean ± SEM; *p < 0.05, **p < 0.01