Fig. 7

HIF-1α deficient mice show exacerbated experimental autoimmune encephalomyelitis. a Clinical score of Mb1^creHif1a^f/f (n = 10) and WT mice (n = 10) immunized with MOG_35-55. b Histopathology sections and quantifications of inflammatory loci (arrows) and demyelinated area (dashed line) in the spinal cord of Mb1^creHif1a^f/f (n = 10) and WT mice (n = 10) showing lymphocyte infiltration (H&E) and demyelination area (LFB). Scale bars, 500 μm. c Representative plots and quantification of CNS-infiltrating cells in Mb1^creHif1a^f/f (n = 7) and WT mice (n = 7) 18 days after induction of EAE. d IL-17, IFN-γ, IL-10, and TGF-β expression by splenocytes isolated from mice as described in c followed by an in vitro re-stimulation with MOG_35-55 (10 μM) for 48 h. e IL-10, TGF-β, and IL-35 production by enriched splenic B cells isolated from Mb1^creHif1a^f/f (n = 5) and WT mice (n = 6) immunized with MOG_35-55 followed by in vitro re-stimulation with MOG_35-55 (10 μM) for 48 h. f–h Representative plots and quantification of IL-17A⁺CD4⁺(Th17), IFN-γ⁺CD4⁺(Th1), CD25⁺Foxp3⁺CD4⁺(Treg), IL-10⁺CD4⁺(Tr1), and IL-10⁺CD19⁺(IL-10⁺B) cells in spleen (f), draining lymph nodes (dLNs) (g), and CNS (h) from Mb1^creHif1a^f/f (n = 7) and WT mice (n = 7) 18 days after induction of EAE. i Representative plots and percentages of IL-23R⁺IL-17A⁺CD4⁺ and GM-CSF⁺IL-17A⁺CD4⁺T cells in spleen and dLNs from Mb1^creHif1a^f/f (n = 6) and WT mice (n = 6) 18 days after induction of EAE. Data are shown as mean ± s.e.m. Pictures are representative of three independent experiments. NS not significant; *P < 0.05, **P < 0.01, and ***P < 0.001 (unpaired, two-tailed Student’s t-test) (see also Supplementary Figure 1)