Pharmacologic inhibition of EphB3 receptor kinase ameliorates EAE

To evaluate the potential of EphB3 as a therapeutic target during CNS inflammation, we induced EAE in B6 WT mice and starting at the peak of the disease we initiated treatment with A38 administered. A38 administration ameliorated EAE, and the transcriptional analysis of the astrocytes and microglia revealed the decreased expression of genes associated to inflammation and neurodegeneration. Astrocytes and microglia were isolated from CNS of mice undergoing EAE and which have been treated with A38 or the vehicle as control. Healthy mice were also included in the comparison.