Joachim Stephanie C, Reichelt Jan, Berneiser Simone, Pfeiffer Norbert, Grus Franz H
Experimental Ophthalmology, Department of Ophthalmology, Johannes Gutenberg University, Langenbeckstrabe 1, 55101 Mainz, Germany.
Graefes Arch Clin Exp Ophthalmol. 2008 Apr;246(4):573-80. doi: 10.1007/s00417-007-0737-8. Epub 2008 Jan 12.
The aim of this study was to gain more information about the possible immunological mechanisms in glaucoma. We analyzed the complex autoantibody patterns against human optic nerve antigens in sera of patients with glaucoma and tried to identify important antigens.
Sera of 133 patients were included: healthy control subjects (n = 44), primary open-angle glaucoma (n = 44), and normal tension glaucoma patients (n = 45). The sera were tested against Western blots of human optic nerve, and antibody bands were visualized with chloronaphthol. IgG antibody patterns were analyzed by multivariate statistical techniques, and the most significant antigens were identified by mass spectrometry (Maldi-TOFTOF).
All subjects, even healthy ones, showed different and complex antibody patterns. Glaucoma groups showed specific up- and down-regulations of antibody reactivities compared to the control group. The multivariate analysis of discriminance found significant differences (P < 0.05) in IgG antibody profiles against human optic nerve antigens between both glaucoma groups and healthy subjects. The identified antigens include: myelin basic protein (up-regulated in the POAG group), glial fibrillary acidic protein (down-regulated in the glaucoma groups), and vimentin (down-regulated in the glaucoma groups in comparison to controls).
Using human optic nerve antigen, we were able to demonstrate that complex IgG autoantibody patterns exist in sera of patients with glaucoma. Large correlations between the given and our previous studies using bovine optic nerve antigens could be seen. Furthermore, anti-myelin basic protein antibodies, which can also be detected in patients with multiple sclerosis, were found in sera of glaucoma patients.
本研究旨在获取更多关于青光眼可能的免疫机制的信息。我们分析了青光眼患者血清中针对人视神经抗原的复杂自身抗体模式,并试图鉴定重要抗原。
纳入133例患者的血清:健康对照者(n = 44)、原发性开角型青光眼患者(n = 44)和正常眼压性青光眼患者(n = 45)。将血清与人视神经的蛋白质印迹进行检测,并用氯萘酚使抗体条带显色。通过多变量统计技术分析IgG抗体模式,并用基质辅助激光解吸电离飞行时间质谱(Maldi-TOFTOF)鉴定最显著的抗原。
所有受试者,甚至健康受试者,均显示出不同且复杂的抗体模式。与对照组相比,青光眼组显示出抗体反应性的特异性上调和下调。判别多变量分析发现,青光眼组和健康受试者之间针对人视神经抗原的IgG抗体谱存在显著差异(P < 0.05)。鉴定出的抗原包括:髓鞘碱性蛋白(在原发性开角型青光眼组中上调)、胶质纤维酸性蛋白(在青光眼组中下调)和波形蛋白(与对照组相比,在青光眼组中下调)。
利用人视神经抗原,我们能够证明青光眼患者血清中存在复杂的IgG自身抗体模式。可以看到本研究结果与我们之前使用牛视神经抗原的研究之间存在很大相关性。此外,在青光眼患者血清中发现了也可在多发性硬化症患者中检测到的抗髓鞘碱性蛋白抗体。