May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Autoimmune Uveitis Induces Loss of Retinal Ganglion Cells: Immune Modulation Rather Than Suppression for Neuroprotection
Author Affiliations & Notes
  • M. Schwartz
    Neurobiology, Weizmann Institute Science, Rehovot, Israel
  • S. Bakalash
    Neurobiology, Weizmann Institute Science, Rehovot, Israel
    Ophthalmology, Schepens eye research Institute, Harvard, Boston, Massachusetts
  • Footnotes
    Commercial Relationships M. Schwartz, None; S. Bakalash, None.
  • Footnotes
    Support None.
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 5213. doi:
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      M. Schwartz, S. Bakalash; Autoimmune Uveitis Induces Loss of Retinal Ganglion Cells: Immune Modulation Rather Than Suppression for Neuroprotection. Invest. Ophthalmol. Vis. Sci. 2007;48(13):5213.

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

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Purpose:: To examine the therapeutic potential of T cell-based vaccination against retinal ganglion cell (RGC) loss under pathological conditions when intraocular pressure is normal.

Methods:: We used two models of transient inflammatory experimental ocular autoimmune diseases, uveitis and optic neuritis, both representing neuropathological conditions induced by inflammation, causing death of RGCs under normal ocular tension conditions. At the peak of disease rats were injected with glatiramer acetate (copolymer-1; Cop-1©), previously identified as a T-cell-based immunomodulatory therapy. As controls, rats were either treated with vehicle or treated with high doses of the steroidal drug methylprednisolone (MP). RGC survival was assessed 2 weeks after the disease had subsided. Immune cells participating in RGC protection were identified by Immunohistochemical analysis.

Results:: Treatment with Cop-1 protected RGCs from degeneration induced by optic neuritis or autoimmune uveitis. Treatment with MP not only failed to reduce RGC loss but even exacerbated it. Immunohistochemical analysis showed that Glatiramer Acetate significantly increased local recruitment of T cells, and activated local macrophages/microglia to express class II major histocompatibility complex (MHC-II) proteins. Treatment with MP, in contrast, reduced activated immune cells to a minimum, and resulted in more RGC loss.Discussion: We suggest that uncontrolled autoimmunity as manifested sometimes in the form of autoimmune diseases, can also be viewed as a possible cause for normal-tension glaucoma. Given the observed lack of benefit of immunosuppression and previous evidence that Cop-1 exerts an immunomodulatory effect, we argue that immune modulation rather than immunosuppression might be the therapeutic strategy of choice for ocular autoimmune diseases as well as for normal-tension glaucoma, whatever the primary cause.

Keywords: immunomodulation/immunoregulation • neuroprotection • uveitis-clinical/animal model 

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