Although these data suggest that MHC class II-restricted antigen presentation by BMECs can contribute to autoimmune neuroinflammation by enhancing CD4 T-cell recruitment into the CNS and several studies localized MHC class II to BMECs in brain or spinal cord sections from rodents suffering from EAE [113], there are no data that causally links MHC class II expression at the BBB to MS pathogenesis. The gene discussed is CD4; the disease is myeloid sarcoma.