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Mandy L Ford, Thandi M Onami, Anne I Sperling, Rafi Ahmed, Brian D Evavold, CD43 Modulates Severity and Onset of Experimental Autoimmune Encephalomyelitis, The Journal of Immunology, Volume 171, Issue 12, December 2003, Pages 6527–6533, https://doi.org/10.4049/jimmunol.171.12.6527
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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.
