September 1995
Volume 36, Issue 10
Free
Articles  |   September 1995
Anti-rhodopsin antibodies in sera from patients with normal-pressure glaucoma.
Author Affiliations
  • C Romano
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63130, USA.
  • D A Barrett
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63130, USA.
  • Z Li
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63130, USA.
  • A Pestronk
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63130, USA.
  • M B Wax
    Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri 63130, USA.
Investigative Ophthalmology & Visual Science September 1995, Vol.36, 1968-1975. doi:
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    • Get Citation

      C Romano, D A Barrett, Z Li, A Pestronk, M B Wax; Anti-rhodopsin antibodies in sera from patients with normal-pressure glaucoma.. Invest. Ophthalmol. Vis. Sci. 1995;36(10):1968-1975.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

PURPOSE: To explore further the potential role autoimmunity may play in the pathogenesis of normal-pressure glaucoma (NPG) in some patients, the authors examined the sera of patients with NPG for the presence of antibodies directed toward retinal antigens. METHODS: Using patient sera, immunoblotting was performed on subcellular fractions of retina, purified bovine rhodopsin, and immunoaffinity-purified recombinant human rhodopsin. A chemiluminescence-enzyme-linked immunosorbent assay (ELISA) to detect anti-rhodopsin antibodies was developed and used. RESULTS: A patient with NPG was found to have a high titer of immunoglobulin M-lambda antibody against a 40-kd retina-specific glycoprotein antigen subsequently identified as rhodopsin. ELISA analysis conducted on sera from 28 patients with NPG and 26 patients with primary open-angle glaucoma (POAG) revealed highly significant differences in anti-rhodopsin antibody activity between these groups (P < 0.0002, Mann-Whitney test). For example, the majority of patients with NPG (19/28; 68%) had anti-rhodopsin antibody activity higher than the highest value obtained from among 26 age-matched patients with POAG. CONCLUSIONS: An elevated anti-rhodopsin antibody count is related to NPG. This may indicate that there is an autoimmune component in the optic neuropathy in these patients. The specific role of these autoantibodies, if any, in the pathogenesis of the disease remains to be determined.

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