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. 2018 Dec 28;116(3):982–987. doi: 10.1073/pnas.1807484116

Fig. 2.

Fig. 2.

Loss of PP2A protects mice from EAE by repressing IL17A production. (A) Mean clinical scores for EAE from each group. (B) Representative histology of the brain and spinal cord [hematoxylin and eosin (H&E) at Left and luxol fast blue (LFB) at Right] of mice after EAE induction (day 19). Arrowheads indicate inflammatory infiltration (Left) and demyelination (Right). (Scale bars: 100 μm.) (C) Number and frequency of mononuclear cells or CD4+ or CD8+ T cells infiltrated into CNS. (D) Flow cytometry of IL17A, IFN-γ, and Foxp3 staining from CNS (Left) or DLN (Right) CD4+ T cells. (E and F) Quantification of IL17A+, IFNγ+, and Foxp3+ CD4+ T cells in CNS (E) or DLN (F). (G) Splenocytes were rechallenged with MOG peptide (5 μg/mL) or control vehicle for 3 d, and cytokine production was measured by ELISA. Each symbol represents an individual mouse (n = 4–6); error bars show mean ± SEM. Data are representative of three independent experiments with similar results. *P < 0.05; **P < 0.01; ***P < 0.001; NS, not significant.