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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: Dual roles of the adenosine A2a receptor in autoimmune neuroinflammation

Fig. 2

Effects of pharmacological A2aR activation in EAE. a Treatment with the A2aR-agonist CGS21680 (0.1 mg/kg) in the early phase of EAE leads to a prevention of disease symptoms (n = 8). Coloured arrows indicate the time points of ex vivo analyses. b Left: treatment with CGS21680 (0.1 mg/kg) in established disease (day 12 post immunization) leads to disease exacerbation (n = 5). Middle: histological analysis of CGS21680-treated EAE shows exacerbated Iba1+ accumulation in the spinal cord tissue (scale bars = 50 μm). Right: quantification of number of inflammatory foci at day 25 post immunization (n = 5). c Spleen cells isolated from vehicle-treated mice at day 7 in early-treatment paradigm (see purple arrow in Fig. 2a) show a higher antigen-specific proliferation capacity than cells isolated from CGS21680-treated mice. Cells isolated from late-stage early-treatment paradigm (orange arrow in Fig. 2a) and late-treatment paradigm (pink arrow in Fig. 2b) do not show differences in antigen-specific proliferation (n = 5). d T cells were transferred from EAE mice treated with CGS21680 or vehicle into naïve, non-immunised, non-treated RAG1-deficient mice (n = 4). e Analysis of migratory capacity towards CXCL12 in the presence or absence of CGS21680 of CD4+ T cells isolated from healthy mice using a Transwell chemotaxis system (data from three independent experiments). *p < 0.05, **p < 0.01, ***p < 0.001

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