J Immunol. 2003 Dec 15;171(12):6527-6533
Ford ML, Onami TM, Sperling AI, Ahmed R, Evavold BD.
Department of Microbiology and Immunology and Emory Vaccine Center, Emory University, Atlanta, GA 30322. Section of Pulmonary and Critical Care Medicine, Department of Medicine, Department of Pathology, and Committee on Immunology, University of Chicago, Chicago, IL 60611.
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-gamma 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 MOG(35-55)-specific T cells in EAE, and identify it as a potential target for therapeutic intervention.