J Neuroimmunol 2003 Mar;136(1-2):34-45
Skundric DS, Zakarian V, Dai R, Lisak RP, Tse HY, James J.
Department of Neurology, Division of Neuroimmunology, Wayne State University School of Medicine, 421 E Canfield, 3141 Elliman Building, 48201, Detroit, MI, USA
To find immune mechanisms underlying relapse regulation, we developed a model of relapsing-remitting experimental autoimmune encephalomyelitis (EAE) in (B6xSJL) F1 (H-2(b/s)) mice by immunization with myelin oligodendrocyte glycoprotein peptide 35-55 (MOG(35-55)) and compared with low/non-relapsing B6 (H-2(b)) mice.In relapsing H-2(b/s) mice, inflammatory lesions scattered throughout the white matter with extensive demyelination, consisted of CD4(+) T and B220(+) B cells with fewer Mac3(+) macrophages.
Memory T cell proliferation to MOG(35-55) was significantly enhanced.
Switch of macrophage chemoattractant protein-1 (MCP-1) production from GFAP(+) astrocytes to CD3(+) T cells was observed.Distinct patterns of inflammation and demyelination, MOG(35-55) memory T cell response and regulation of MCP-1 are associated with relapsing H-2(b/s) phenotype.