Background: 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.
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 secondary 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. 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.
Conclusions: 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.
Keywords: acute angle-closure glaucoma; autoantibody repertoire; immune response; intraocular pressure.
© 2016 Royal Australian and New Zealand College of Ophthalmologists.