Skip to main content
Figure 3 | Journal of Neuroinflammation

Figure 3

From: Experimental mouse model of optic neuritis with inflammatory demyelination produced by passive transfer of neuromyelitis optica-immunoglobulin G

Figure 3

Continuous perichiasmal infusion of neuromyelitis optica immunoglobulin G antibody and complement produces complement-dependent, neuromyelitis optica-like optic neuritis. (A) (Top) Micrographs showing aquaporin-4 (AQP4), glial fibrillary acidic protein (GFAP), myelin basic protein (MBP) and neurofilament (NF) immunoreactivity in the optic nerve after 3-days continuous perichiasmal infusion of complement with neuromyelitis optica immunoglobulin G antibody (NMO-IgG) or control IgG in wild-type mice and NMO-IgG in AQP4-/- mice. White dashed line demarcates area with loss of immunofluorescence. (Bottom) Higher magnification of yellow boxes. (B) (Top) AQP4, GFAP, MBP and NF immunofluorescence in the optic nerve after 3-days continuous perichiasmal infusion of (left) NMO-IgGCDC+ with or without complement in wild-type mice or (right) complement with control IgG or NMO-IgG in CD59-/- mice. White dashed line demarcates region with loss of immunofluorescence. (Bottom) Higher magnification of yellow boxes. (C) Hematoxylin and eosin staining of the optic nerve after 3-days continuous perichiasmal infusion in wild-type mice of control IgG or NMO-IgG or NMO-IgGCDC+, with or without complement. HC, human complement.

Back to article page