| First Author | Ford ML | Year | 2003 |
| Journal | J Immunol | Volume | 171 |
| Issue | 12 | Pages | 6527-33 |
| PubMed ID | 14662853 | Mgi Jnum | J:86932 |
| Mgi Id | MGI:2682476 | Doi | 10.4049/jimmunol.171.12.6527 |
| Citation | Ford ML, et al. (2003) CD43 modulates severity and onset of experimental autoimmune encephalomyelitis. J Immunol 171(12):6527-33 |
| abstractText | 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. |
