[Autoimmune mechanisms in molecular pathology of glaucomatous optic neuropathy]

Glaucomatous optic neuropathy is characterized by loss of retinal ganglion cells and their axons, excavated appearance of the optic nerve head, and progressive loss of visual field sensitivity. In terms of pathology of the glaucomatous optic neuropathy, observations suggest retinal ganglion cell death by apoptosis. Deprivation of neurotrophic factors, ischemia, chronic elevation of glutamate, and disorganized nitric oxide metabolism have been suspected to be mechanisms triggering apoptosis. Another recent suggestion is that autoantibodies directed toward retinal antigens may be involved in facilitating apoptotic cell death in some glaucoma patients.

We summarized previous reports dealing with the relationship between glaucoma etiology and autoimmune responses, and investigated the contribution of autoimmune factors in glaucomatous optic neuropathy using electrophysiological and biochemical methods.

We found serum anti-neuron specific enolase(NSE) antibody in approximately 20% of our glaucoma patients. In primary open angle glaucoma, maximum and mean intraocular pressures in antibody positive patients were significantly or relatively lower than pressures in antibody negative patients. In addition, we also found that apoptotic cell death of retinal ganglion cells was induced in rat eyes by intravitreal administration of purified anti-NSE antibody.

As suggested by previous reports, autoimmune response is one of the mechanisms related to glaucoma etiology and NSE may have an important function as an autoantigen.