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Figure 2 | Journal of Neuroinflammation

Figure 2

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

Figure 2

Continuous perichiasmal infusion of neuromyelitis optica immunoglobulin G antibody and complement leads to aquaporin-4 loss and complement activation in optic nerve. (A) (Left) Three-day continuous intracranial perichiasmal infusion of neuromyelitis optica immunoglobulin G antibody (NMO-IgG) and human complement was done by implantation of an osmostic pump. (Right) Area of diffusion in optic chiasm and brain of an infused blue dye (dashed line). (B) Immunofluorescence showing binding of NMO-IgG to aquaporin-4 (AQP4) in brain around the needle tract (white line) at 3-days after infusion of NMO-IgG or control IgG and complement. (C) AQP4 immunofluorescence, hematoxylin and eosin (H&E) staining and NMO-IgG immunofluorescence of the optic nerve. Dashed lines show lesion or area of NMO-IgG deposition. (D) Immunofluorescence showing AQP4 loss, NMO-IgG deposition and complement activation (C5b-9, arrows) in the optic nerve after infusion of NMO-IgG as in (A). White dashed lines demarcate the lesion.

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Journal of Neuroinflammation

ISSN: 1742-2094