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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: α-Synuclein deficiency promotes neuroinflammation by increasing Th1 cell-mediated immune responses

Fig. 2

Earlier symptom onset in aSyn−/− mice accompanied by increased spinal cord infiltration of Th1 cells during EAE. a Percentage of mice without symptoms during the onset phase of EAE is shown. The aSyn−/− cohort (dashed line) exhibited significantly less disease-free mice compared to the aSyn+/+ cohort (solid line) (n = 15/16; *p < 0.05). b aSyn−/− mice (white dots, dashed line) showed a significantly more severe clinical course during the initial phase of EAE than aSyn+/+ mice (black dots, solid line) (n = 15/16; **p < 0.01). Symptom severity at disease peak was not different between both groups. c Western blot analysis reveals the presence of α-synuclein (α-syn) in antigen-presenting cells (CD11b+ and CD11c+) and CD4+ T cells isolated from the spleen of aSyn+/+ mice. Spinal cord (SC) lysates of aSyn+/+ and aSyn−/− mice were loaded as positive and negative controls for α-synuclein immunoreactivity. d Representative contour plots of ex vivo flow cytometry to determine frequencies of IL-17A+ and/or IFN-γ+ cells within the spinal cord of aSyn+/+ (upper panel) and aSyn−/− (lower panel) mice 2 days after symptom onset of EAE are depicted. e In the spinal cord of aSyn−/− mice (gray bars), there were significantly higher frequencies of IFN-γ+ Th1 and IFN-γ+/IL-17A+ Th1/Th17 cells as compared to aSyn+/+ mice (black bars) (n = 4; *p < 0.05, **p < 0.01). f Frequency of regulatory T cells was lower in aSyn−/− mice (n = 4; **p < 0.01). g There was no difference in the frequency of antigen-presenting cells (n = 4; p > 0.05)

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