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AbstractDO.05.03 Retinal ganglion cell degeneration through immunization with ocular antigens in a glaucoma animal model Reichmann J., Joachim S. C., Gramlich O. W., Pfeiffer N., Grus F. H.
Experimentelle Ophthalmologie, Universitäts-Augenklinik, Johannes Gutenberg-Universität, Mainz Objective: Antibody patterns in aqueous humor and sera of glaucoma patients provide hints for changes in the autoimmunity. In order to test the hypothesis that autoimmune mechanisms are involved in the pathogenesis of glaucoma, we established an Experimental Autoimmune Glaucoma (EAG) animal model through immunization with ocular antigens. The aim of this study is to find out if immunization with myelin basic protein (MBP) and vimentin can cause retinal ganglion cell (RGC) loss.
Methods: 33 Lewis rats were divided into 3 group (n=11 per group). Two groups were immunized with either MBP or vimentin plus Freunds adjuvant and pertussis toxin. The control animals got injections of pertussis toxin and Freunds adjuvant. All animals received booster immunizations after 4 and 8 weeks with 50% of the initial dose and were euthanized after 10 weeks. Intraocular pressure (IOP) was measured in all animals before the study and after 2, 4, 8, and 10 weeks after immunization and fundus pictures were taken at the same time. After the study the eyes were enucleated and fixed in 4% paraformaldehyde. The retinal flatmounts were stained with Kresylblue to detect retinal ganglion cells and counted in 40x magnification.
Results: No significant changes in IOP were observed, neither during the course of the study, nor between immunized and non-immunized animals. No pathological changes could be observed on the fundi. The significant RGC loss occurred in animals immunized with MBP (P=0.0001) as well as in animals immunized with vimentin (P=0.0002) after 10 weeks.
Conclusions: MBP (a myelin sheath component) and vimentin (a cytoskeletal protein) are two important retinal structures. The results showed RGC loss after immunizing with these antigens, which could be an indication for a damaging effect of a high concentration of autoantibodies against structural proteins of the retina.
Support: Boehringer Ingelheim Foundation, MAIFOR
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