Involvement of junctional adhesion molecules in the pathogenesis of experimental autoimmune encephalomyelitis

Abstract

In the pathogenesis of multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE) leukocyte migration into the central nervous system (CNS) has been defined as key-event. Circulating leukocytes enter the CNS by crossing either the highly specialized endothelium forming the blood–brain-barrier (BBB) or the epithelium establishing the blood–cerebrospinal fluid barrier (BCSFB). Junctional adhesion molecule (JAM)-A is expressed in tight junctions of both barriers as well as by different leukocyte subsets while JAM-B is exclusively expressed by endothelial cells.