To distinguish the role of general neuroinflammation and thus increased endothelial adhesion molecule expression from that of endothelial MHC-class I restricted Ag presentation on OT-I cell crawling speed on the BBB we next investigated the interaction of CMFDA-labeled effector OT-I cells with the spinal cord microvessels in C57BL/6 J mice during the peak of experimental autoimmune encephalomyelitis (EAE), where neuroinflammation is induced by autoaggressive myelin-specific CD4+ T cells. The gene discussed is CD4; the disease is experimental autoimmune encephalomyelitis.