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Editors Selection IGR 15-2
Basic Research: HSP27 immunization and RGC loss
Comment by Gülgün Tezel on:
24825 Complex antibody profile changes in an experimental autoimmune glaucoma animal model, Joachim SC; Grus FH; Kraft D et al., Investigative Ophthalmology and Visual Science, 2009; 50: 4734-4742
Immunization of rats with HSP27 has been reported to cause retinal ganglion cell (RGC) loss. Similar to previous observations, Joachim et al. (1436) detected a lower RGC density in HSP27-immunized rats relative to controls as assessed by counting Brn3a-labeled cells in retinal flatmounts. The authors also analyzed whether HSP27 immunization affects systemic antibody patterns in these animals. Two and four weeks after immunization, they detected a significant difference in serum immunoreactivity to bovine retinal proteins between immunized rats and controls, which exhibited either an increase or decrease in serum antibody titers. Complex antibody profiles were analyzed using Western blots of serum samples, and mass spectrometric analysis identified HSP27, HSP90, α-enolase, and glyceraldehyde-3-phosphate dehydrogenase as most prominent antigens.
The IOP-independent RGC loss detected after HSP27 immunization and alterations detected in serum antibody profiles in immunized animals bring about many questions: Does this experimental model properly simulate conditions in human glaucoma? What is the statistical power of observations? What is the cause of RGC loss in HSP27-immunized animals? Is the RGC loss detected after HSP27 immunization immune-mediated? Is the immune response detected in immunized animals specific to the retina, and if so, what does determine a specific response in these animals following immunization with a non-specific antigen? Does the neurodegenerative injury include innate and/or adaptive components of the immune system? May this disease be transferred to naïve animals? Do serum antibodies play a causative role in RGC loss? What is the importance of the decreased serum immunoreactivity detected in immunized animals? What is the role of molecular mimicry and cross-reactivity in detected serum immunoreactivities?
Ongoing studies are hoped to answer these important questions so that the ability to produce an experimental autoimmune disease model will serve as a critical step to validate and further explore the immunogenic component of neurodegenerative injury in glaucoma.
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