Figure 2From: Extracellular adenosine signaling induces CX3CL1 expression in the brain to promote experimental autoimmune encephalomyelitis CX3CL1 upregulation within the brain during EAE is associated with A2A adenosine receptor signaling. (A) CX3CL1 gene expression (relative to DMSO vehicle) in the brains of wild type mice following 4 hour A2A adenosine receptor agonist CGS21680 treatment as determined by quantitative real-time PCR. Error bars represent the s.e.m.; n ≥ 3 mice / treatment. Significant differences (P < 0.05, *; P < 0.001, ***) are indicated as determined by the Student’s t-test. (B) EAE disease profile in wild type mice given either the A2A adenosine receptor antagonist SCH58261 (1 mg/kg, open diamonds, n = 8; 5 mg/kg, open triangles, n = 7) or a vehicle control (n = 8). Error bars represent the s.e.m. EAE data is combined from 2 separate experiments. (C) CD45 and CD4 stained frozen brain sections (hippocampal area) from day 10 post-EAE induction SCH58261 and vehicle treated wild type mice. Positively stained cells (red) are shown against a hematoxylin counterstain (blue). Black scale bars represent 50 μm. (D) Brain CX3CL1 expression over time in wild type mice induced to develop EAE and given either SCH58261 or a vehicle control as determined by quantitative real-time PCR. Error bars represent the s.e.m. Significant differences (P < 0.001, ***) are indicated as determined by the Student’s t-test.Back to article page