Lorenz Katrin, Beck Sabine, Keilani Munir M, Wasielica-Poslednik Joanna, Pfeiffer Norbert, Grus Franz H
Department of Experimental Ophthalmology, University Medical Center, Johannes Gutenberg-University, Mainz, Germany.
Department of Pharmacy and Biochemistry, Johannes Gutenberg-University Mainz, Germany.
Clin Exp Ophthalmol. 2017 Apr;45(3):280-287. doi: 10.1111/ceo.12864. Epub 2017 Feb 6.
The aim of our investigation was to analyze the autoantibody -reactivities of patients after acute angle-closure glaucoma (AACG) by means of a protein microarray approach to identify intraocular pressure(IOP)-dependent antibodies.
Collected sera from different study time points (AACG n = 6, 0, 2, 4 and 12 weeks) and control group (CTRL n = 11, 0 and 12 weeks) were analyzed. Protein-microarrays were incubated with sera, and occurring immunoreactivities were visualized with fluorescence labeled secondary antibodies. To detect changes, spot intensities were digitized and compared with statistical techniques.
Three autoantibodies with significant level-alteration in the time course of the survey could be identified. Immunoreactivities to heat shock 27-kDa protein (HSP27), tubulin-tyrosine ligase-like protein 12 (TTLL12), and neuron-specific enolase (NSE) show an increasing linear trend from week 0 up to week 12 with a positive correlation coefficient (P ≤ 0.05, r ≥ 0.4). In the CTRL- group, no significant alterations could be detected in corresponding autoantibody-level. Analysis of variance revealed significant changes of antibody-level between certain time points (anti-HSP27 antibody [week 0 vs. 2], anti-TTLL12 antibody [week 0 vs. 12], and anti-NSE antibody [week 4 vs. 12] [P ≤ 0.05, respectively]) in AACG group.
With this autoantibodies profiling approach, we were able to detect autoimmune reactivities in sera of patients without former indication for glaucomatous damage after rise of IOP due to AACG attack. After further validation in subsequent studies, this autoantibodies could give further insights into the pathogenesis of glaucoma and could possibly help to understand the effect of IOP on glaucomatous optic neuropathy.
我们研究的目的是通过蛋白质微阵列方法分析急性闭角型青光眼（AACG）患者的自身抗体反应性，以识别眼压（IOP）依赖性抗体。
分析了来自不同研究时间点（AACG组n = 6，分别为0、2、4和12周）和对照组（CTRL组n = 11，分别为0和12周）的血清。将蛋白质微阵列与血清孵育，并用荧光标记的二抗观察出现的免疫反应性。为了检测变化，将斑点强度数字化并采用统计技术进行比较。
在调查过程中可识别出三种自身抗体水平有显著变化。对热休克27 kDa蛋白（HSP27）、微管蛋白酪氨酸连接酶样蛋白12（TTLL12）和神经元特异性烯醇化酶（NSE）的免疫反应性从第0周直至第12周呈线性上升趋势，相关系数为正（P≤0.05，r≥0.4）。在CTRL组中，相应自身抗体水平未检测到显著变化。方差分析显示，AACG组某些时间点之间抗体水平有显著变化（抗HSP27抗体[第0周与第2周]、抗TTLL12抗体[第0周与第12周]以及抗NSE抗体[第4周与第12周][P均≤0.05]）。
通过这种自身抗体分析方法，我们能够在因AACG发作导致眼压升高后，在既往无青光眼损伤迹象的患者血清中检测到自身免疫反应性。在后续研究中进一步验证后，这些自身抗体可能会为青光眼的发病机制提供更多见解，并可能有助于理解眼压对青光眼性视神经病变的影响。
