April 2010
Volume 51, Issue 13
ARVO Annual Meeting Abstract  |   April 2010
Retinal Ganglion Hypersensitivity: A 56 kd Protein Antigen of Interest
Author Affiliations & Notes
  • C. E. Thirkill
    Ocular Immunology,, Univ of California - Davis, Davis, California
  • Footnotes
    Commercial Relationships  C.E. Thirkill, Athena Diagnostics, P.
  • Footnotes
    Support  RPB and NEI Core Grant 1 P30 EY12576-05
Investigative Ophthalmology & Visual Science April 2010, Vol.51, 4816. doi:
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      C. E. Thirkill; Retinal Ganglion Hypersensitivity: A 56 kd Protein Antigen of Interest. Invest. Ophthalmol. Vis. Sci. 2010;51(13):4816.

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

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Purpose: : Immunologically distinct subsets of glaucoma patients produce antibodies reactive with retinal ganglion cells (RGCs). This abnormality may prove significant to the vision loss of these subgroups due to the recognized loss of RGCs in the pathologic process of the glaucomas, and the possibility of autoimmune involvement.

Methods: : Patients were selected for antibody activity with RGCs, visualized by Indirect Fluorescent Antibody assays (IFA) on sectioned rhesus monkey eye. A viable culture of human RGCs was established, (with IRB approval) , to represent the target tissue of interest. The established culture of rodent retinal ganglion cells (RGC-5) was used as a comparison control. Western blots on extracts of cultured RGCs were used to identify the relative size of the antigen(s) involved. IFA enabled the identification of the site of expression of the antigen within monolayers of in vitro cultivated human RGCs.

Results: : Findings implicate an immunologic commonality involving a 56 kd protein antigen, expressed within the cytoplasm of RGCs.

Conclusions: : Heat shock proteins are suspect autoantigens in several autoimmune diseases, including RGC hypersensitivity, but they have little tissue specificity. Preliminary findings indicate the 56 kd RGC antigen is tissue-specific. Theoretically, since hyperactive patients are all producing autoantibodies against the same 56 kd antigen, they must have all experienced the same antigenic stimulation ! ‘Is it from an infection ?’ This supposition extends on knowledge of post-infective polyneuritis, and other neuropathies that manifest as the sequelae of a variety of infectious diseases, and immunizations. Access to in vitro human RGCs permits further inquiry; 'are these cells, or the 56 kd antigen alone capable of inciting a corresponding autoimmune reaction in lab rats', a form of ‘Experimental Autoimmune Retinal Gangliopathy’ of use in future research and, ‘are the patient’s anti-56 kd antibodies inhibitory to the viability, and function of cultured human RGCs ?’

Keywords: autoimmune disease • ganglion cells • detection 

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