An increase in DICAM-expressing Th17 CD4+ T cells and the upregulation of the DICAM ligand on the brain endothelial cells upon inflammation and in MS lesions have been observed, and monoclonal antibodies against DICAM have been shown to reduce Th17 cell trafficking across the blood–brain barrier both in vitro and in vivo and to ameliorate both relapsing and progressive EAE [37]. Here, CD4 is linked to myeloid sarcoma.