Grus F H
Universitäts-Augenklinik, Experimentelle Ophthalmologie, Mainz.
Klin Monbl Augenheilkd. 2010 Feb;227(2):114-9. doi: 10.1055/s-0029-1245150. Epub 2010 Feb 12.
Elevated intraocular pressure does not explain glaucoma in all patients, but there is information that autoimmune mechanisms may be involved in this disorder. We have demonstrated in several studies that glaucoma patients reveal changes in their immune reactivities against ocular antigens. The mechanisms of these reactivities are still widely unknown, but oxidative pathways could play a major role. There is evidence that free radicals are able to alter the ability of glial cells to be recognized as antigens. Furthermore, one can assume that during the aging process posttranslational changes, e. g., oxidation of ocular antigens increase with age. It is feasible that these changed antigens may trigger such changes. in an autoimmune glaucoma animal model we have shown that immunological processes after immunisation can lead to a loss of retinal ganglion cells. Considering that these changes in natural autoimmunity can be found consistently amongst different study populations, it might be a promising new tool for glaucoma diagnosis and new therapeutic immunomodulating options.
眼压升高并不能解释所有患者的青光眼病因，但有信息表明自身免疫机制可能参与了这种疾病。我们在多项研究中证明，青光眼患者针对眼部抗原的免疫反应性会发生变化。这些反应的机制仍然广为人知，但氧化途径可能起主要作用。有证据表明自由基能够改变神经胶质细胞被识别为抗原的能力。此外，可以推测在衰老过程中，翻译后修饰变化，例如眼部抗原的氧化会随着年龄增长而增加。这些变化的抗原可能引发此类变化是可行的。在一个自身免疫性青光眼动物模型中，我们已经表明免疫接种后的免疫过程会导致视网膜神经节细胞的丢失。考虑到在不同研究人群中始终能发现自然自身免疫的这些变化，它可能是青光眼诊断的一种有前景的新工具以及新的治疗性免疫调节选择。
