Kristina Berve, Julia Michel, Silvia Tietz, Claudia Blatti, Daniela Ivan, Gaby Enzmann, Ruth Lyck, Urban Deutsch, Giuseppe Locatelli, Britta Engelhardt
In multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE), early pathological features include immune cell infiltration into the central nervous system (CNS) and blood-brain barrier (BBB) disruption. We investigated the role of junctional adhesion molecule-A (JAM-A), a tight junction protein, in active EAE (aEAE) pathogenesis. Our study confirms JAM-A expression at the blood-brain barrier and its luminal redistribution during aEAE. JAM-A deficient (JAM-A-/- ) C57BL/6J mice exhibited milder aEAE, unrelated to myelin oligodendrocyte glycoprotein-specific CD4+ T-cell priming...
April 2, 2024: European Journal of Immunology