Although we cannot exclude other factors such as cytokines released by activated microglia/macrophages that are present in the CNS after multiple i.n. GAS infections (55), or the ability of GAS antibodies to break down endothelial cell junctions, the high degree of correlation between the presence of bacterial-specific Th17 cells and BBB leakage suggests that IL-17 likely contributes to BBB dysfunction in a similar fashion as in EAE/MS (55, 115). This evidence concerns the gene IL17A and myeloid sarcoma.