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Editors Selection IGR 7-1
Basic Research: Auto-immune model of RGC loss
Comment by Gülgün Tezel on:
48120 Autoreactive antibodies and loss of retinal ganglion cells in rats induced by immunization with ocular antigens, Laspas P; Gramlich OW; Müller HD et al., Investigative Ophthalmology and Visual Science, 2011; 52: 8835-8848
In continuation of previous work, Laspas et al. (1783) aimed to generate an experimental autoimmune animal model of retinal ganglion cell (RGC) loss by immunization with glaucoma-related antigens. Despite the lack of intraocular pressure increase or fundoscopic alterations, rats injected with optic nerve antigens exhibited increased serum antibodies and a significant RGC loss four weeks after immunization. However, in the control group immunized with keratin, no RGC loss was detectable. Histological examination of retina, optic nerve, and brain sections supported antibody accumulation in animals immunized with optic nerve antigens. In addition, retina and optic nerve tissues in these animals exhibited cellular infiltrates and microglial activation, supportive of an inflammatory process. The authors concluded based on these findings that antibody-mediated systemic autoimmunity is involved in RGC loss in this experimental model. Antibody production after antigen immunization is not unexpected. However, histological alterations and RGC loss detected after immunization with optic nerve antigens support the damaging potential of immune system reactivity, although the outcome of multi-antigen immunization might have been more widespread. Findings of this study bring about many questions that motivate further research to improve our understanding of the immunogenic component of glaucomatous neurodegeneration. What should be the ultimate experimental approach to improve the representative value of sampled RGC counts and the statistical power of data analysis? Does axonal injury accompany RGC loss? What is the time-course of inflammatory responses, antibody production, and neuronal loss in immunized animals? What is the mechanism behind RGC loss in animals immunized with optic nerve antigens? What are the characteristics of immunogenic injury to determine whether it is organ-specific? Is the neuronal injury antigen-specific and antibody-mediated, or does it reflect collateral injury from innate cellular responses? Are T cells involved in this experimental model? May the disease be transferred to naïve animals? Does the experimental model properly simulate conditions in human glaucoma in which local and systemic stressors, and genetic/epigenetic risk factors may change immune homeostasis and increase the susceptibility of RGCs to an immunogenic injury?
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