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Editors Selection IGR 10-2

Basic research: Immune system and glaucoma

Comment by Gülgün Tezel on:

12131 Autoantibodies in patients with glaucoma: a comparison of IgG serum antibodies against retinal, optic nerve, and optic nerve head antigens, Joachim SC; Pfeiffer N; Grus FH, Graefe's Archive for Clinical and Experimental Ophthalmology, 2005; 243: 817-823

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There are conflicting aspects of the immune system in glaucoma, including both the benefit of 'protective immunity' and the risk of inducing an 'auto-immune neurodegenerative disease'. A normal immune regulatory process for host surveillance is involved in glaucoma so that the injured tissue is cleaned by a healthy immune system. However, growing evidence through the past decade also suggests that the immune system plays a potential role in the neurodegenerative process of glaucoma, at least in some patients. The evidence includes elevated serum titers of antibodies to many retina and optic nerve antigens, such as heat shock proteins, rhodopsin, glucosaminoglacans enolase, and glutathione-S-transferase. The findings of Joachim et al. (6) support the elevated serum antibodies in glaucoma patients. Increased serum antibodies may simply reflect an immune response to tissue injury in glaucomatous eyes. However, considerable evidence supports an autoimmune component of neurodegeneration in glaucoma, which may result from aberrant processing of an immune signal in such a way that T-cell-mediated, antibody-mediated, or 'mimicked' autoimmunity eventually contributes to neuronal damage. Obviously, the tissue stress and the neuronal damage in glaucomatous eyes are important factors serving as immunostimulatory signals, which ultimately determine the critical balance between diverse roles of the immune system in glaucoma. Similar to previous studies, Joachim et al. detected a differential pattern of serum immunoreactivity between patients with primary open-angle glaucoma and normal-pressure glaucoma. However, since primary open-angle glaucoma and normal-pressure glaucoma are not entirely different diseases, the interpretation of such an observation is not simple. In addition, individual differences, also detected by Joachim et al., signify the importance of individual factors in determining serum immunoreactivity to ocular antigens, which make the interpretation of findings more complex. We hope that continued efforts will facilitate a better understanding of the role of the immune system in glaucoma and contribute to the identification of biomarkers and improved treatment strategies for glaucomatous neurodegeneration.

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