CD43 Modulates Severity and Onset of Experimental Autoimmune Encephalomyelitis

Abstract

Experimental autoimmune encephalomyelitis (EAE) is a mouse model of multiple sclerosis characterized by infiltration of activated CD4+ T lymphocytes into tissues of the CNS. This study investigated the role of CD43 in the induction and progression of EAE. Results demonstrate that CD43-deficient mice have reduced and delayed clinical and histological disease severity relative to CD43+/+ mice. This reduction was characterized by decreased CD4+ T cell infiltration of the CNS of CD43−/− mice but similar numbers of Ag-specific T cells in the periphery, suggesting a defect in T cell trafficking to the CNS. The absence of CD43 also affected cytokine production, as myelin oligodendrocyte glycoprotein (MOG) 35–55-specific CD43−/− CD4+ T cells exhibited reduced IFN-γ and increased IL-4 production. CD43−/− CD4+ MOG-primed T cells exhibited reduced encephalitogenicity relative to CD43+/+ cells upon adoptive transfer into naive recipients. These results suggest a role for CD43 in the differentiation and migration of MOG35–55-specific T cells in EAE, and identify it as a potential target for therapeutic intervention.