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Editors Selection IGR 7-1

Basic research: Immune system in glaucoma

Comment by Gülgün Tezel on:

20872 Analysis of autoantibodies against human retinal antigens in sera of patients with glaucoma and ocular hypertension, Reichelt J; Joachim SC; Pfeiffer N et al., Current Eye Research, 2008; 33: 253-261

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The immune system functions in the maintenance of the central nervous system by providing tissue cleaning and limiting neurodegenerative consequences of stressful conditions. However, a failure in the regulation of immunity resulting from increased levels of risk factors may turn protective immunity into an autoimmune neurodegenerative process. Growing evidence now supports that both the innate and adaptive components of the immune system exhibit aberrant activity in glaucoma. It is evident that glaucomatous tissue stress and injury serve as an immunostimulatory signal, thereby eliciting an activated immune response; and a stress-related failure in immunoregulatory mechanisms may lead to a sequence of events with neurodegenerative consequences. The evidence supporting aberrant immune activity in glaucoma includes an increasing number of studies reporting serum antibodies against different retina and optic nerve proteins. By studying sera collected from 179 patients, findings of Reichelt et al. (561) detected complex antibody patterns against human retinal proteins. Their observations exhibit large correlations with previous findings obtained by testing serum antibodies against bovine retinal proteins.
Mass spectrometric analysis of western blot bands identified three immunoreactive bands at 12, 29, and 49 kDa as Histone H4, cellular retinaldehyde-binding protein, and retinal S-antigen.

Serum auto-antibodies, apart from being of potential pathogenic importance, may also serve as biomarkers of the disease

Unfortunately, the relevance of these proteins to glaucoma is unclear, as is the importance of many other serum antibodies previously detected in the glaucoma patient sera. Whether these serum antibodies play a causative role or only reflect an epiphenomenon of the disease remains to be clarified. Increased auto-antibody production may result from normal immunoregulatory processes for host surveillance, and increased serum antibodies may represent the adaptive arm of an immune response to neutralize proteins whose expression or exposure is increased during glaucomatous tissue stress or injury. It is also unclear whether the serum immunoreactivities detected may result from molecular mimicry through which an inappropriate host response is mistakenly directed to a self protein sharing a sequence homology to a specific microbial component. Besides their potential pathogenic importance, serum auto-antibodies may also serve as biomarkers of the disease, and ongoing efforts of this group promise potential applications.

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