Experimental Ophthalmology, Department of Ophthalmology, University Medical Center of the Johannes Gutewnberg University, Langenbeckstr. 1, 55131 Mainz, Germany.
Prog Retin Eye Res. 2013 Sep;36:199-216. doi: 10.1016/j.preteyeres.2013.02.003. Epub 2013 Mar 27.
Glaucoma is a chronic neurodegenerative disease and one of the leading causes of blindness. Several risk factors have been described, e.g. an elevated intraocular pressure (IOP), oxidative stress or mitochondrial dysfunction. Additionally, alterations in serum antibody profiles of glaucoma patients, upregulation (e.g. anti-HSP60, anti-MBP) and downregulation (e.g. anti-14-3-3), have been described, but it still remains elusive if the autoantibodies seen in glaucoma are an epiphenomenon or causative. However, it is known that elicited autoimmunity causes retinal ganglion cell loss resulting in glaucomatous-like damage and according to the autoaggressive nature of some autoantibodies we found antibody deposits in human glaucomatous retinae in a pro-inflammatory environment. Furthermore, glaucomatous serum has the potential to influence neuroretinal cell regulatory processes. Importantly, we demonstrate that some autoantibodies hold neuroprotective potential for neuroretinal cells. The protective nature of autoantibodies and the molecular mechanisms underlying the very sensitive equilibrium between autoaggression and protection remain subject of future examinations and offer promising target sites for new therapeutic approaches. Additionally, the changes in antibody profiles could be used as highly sensitive and specific marker for diagnostics purposes. Early diagnosis and intervention in risk patients would offer the chance of early treatment and to slow down the progression of glaucoma and delay the resulting blindness.
青光眼是一种慢性神经退行性疾病，也是导致失明的主要原因之一。已经描述了几种风险因素，例如眼内压升高（IOP）、氧化应激或线粒体功能障碍。此外，青光眼患者的血清抗体谱发生改变，上调（例如抗 HSP60、抗 MBP）和下调（例如抗 14-3-3），但仍不清楚青光眼患者中所见的自身抗体是一种现象还是病因。然而，众所周知，引发的自身免疫会导致视网膜神经节细胞丢失，从而导致类似青光眼的损伤，根据一些自身抗体的自身攻击性，我们在炎症前环境中发现了人类青光眼视网膜中的抗体沉积。此外，青光眼血清有可能影响神经视网膜细胞的调节过程。重要的是，我们证明了一些自身抗体对神经视网膜细胞具有神经保护作用。自身抗体的保护性质以及自身攻击和保护之间非常敏感的平衡的分子机制仍然是未来研究的主题，并为新的治疗方法提供了有前途的靶点。此外，抗体谱的变化可用作诊断目的的高度敏感和特异性标志物。对高危患者进行早期诊断和干预将提供早期治疗的机会，减缓青光眼的进展并延迟由此导致的失明。
