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RESEARCH PRODUCT

Course of serum autoantibodies in patients after acute angle-closure glaucoma attack

Franz H. GrusNorbert PfeifferSabine BeckJoanna Wasielica-poslednikMunir M. KeilaniKatrin Lorenz

subject

0301 basic medicineIntraocular pressuremedicine.medical_specialtybiologyMicroarraybusiness.industryEnolaseAutoantibodyGlaucomamedicine.diseasePathogenesis03 medical and health sciencesOphthalmology030104 developmental biology0302 clinical medicineOphthalmologyImmunologymedicinebiology.proteinAnalysis of varianceAntibodybusiness030217 neurology & neurosurgery

description

Background The aim of our current 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. Methods 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 anti-human-IgG antibodies. To detect changes, spot intensities were digitized and compared with statistical techniques. Results Three autoantibodies with significant level-alteration in the time course of the survey could be identified. Immunoreactivites to HSP27 (heat shock 27 kDa protein), TTLL12 (Tubulin-tyrosine ligase-like protein 12) and NSE (neuron-specific enolase) 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. Conclusion 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 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. This article is protected by copyright. All rights reserved.

https://doi.org/10.1111/ceo.12864