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Immunological Mechanisms in Glaucoma

Laufzeit: 01.01.2008 - 31.12.2009

Kurzfassung


Glaucoma, one of the main causes of blindness worldwide, is responsible for progressive loss of axons of retinal ganglion cells, atrophy of the optic nerve and gradual loss of visual field.
Several studies analyzed antibodies in sera of glaucoma patients. These studies showed antibodies against ocular antigens, such as heat shock proteins (HSPs), γ-enolase and fodrin. The Experimental Ophthalmology Unit could show significant differences between antibody profiles against ocular antigens of...
Glaucoma, one of the main causes of blindness worldwide, is responsible for progressive loss of axons of retinal ganglion cells, atrophy of the optic nerve and gradual loss of visual field.
Several studies analyzed antibodies in sera of glaucoma patients. These studies showed antibodies against ocular antigens, such as heat shock proteins (HSPs), γ-enolase and fodrin. The Experimental Ophthalmology Unit could show significant differences between antibody profiles against ocular antigens of patients with glaucoma and healthy subjects. These findings suggest that autoimmunity plays a role in the disease process, at least in some patients with glaucoma.
Proof that antibodies are involved in the pathogenesis of a disease is normally achieved by animal models in which the disease is elicited by selective immunogens.
Currently all “glaucoma” animal models are based on direct damage of the retinal ganglion cells or optic nerve. Several models elevate IOP, e.g. ischemia\reperfusion model or chronic hypertension model, other models use optic nerve crush to cause damage. None of these models is suitable to analyze a possible immunological involvement in the glaucoma pathogenesis.
Therefore, an Experimental Autoimmune Glaucoma model was developed, which will be studied in more detail now.
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