Abstract
Purpose:
Agonistic Autoantibodies (AAB) against G protein coupled receptors (GPCR) are found in several human diseases (e. g. Asthma, arterial hypertension). β2-adrenergic receptors are involved in the regulation of aqueous humor dynamics. The aim of this study was to investigate the distribution of agonistic β2-adrenergic receptor autoantibodies (β2-AABs) in glaucoma suspects and glaucoma patients.
Methods:
92 probands were included (25 normals, 32 OHTs, 12 pre-perimetric POAGs, 23 POAGs; Erlangen Glaucoma Registry, ISSN 2191-5008, CS-2011; NTC00494923). All patients underwent complete ophthalmological examinations including examinations with Octopus G1 program. Serums probes of all patients were analyzed of β2-AABs using a bioassay (1). In this assay the alteration of the beating rate of spontaneously beating cultured neonatal rat cardiomyocytes, expressing GPCR, due to the applied serum level of AABs, is counted. Statistical analysis was done using non-parametric U-Test. The protocol was approved by the local Ethics Committee (3457).
Results:
All normals showed β2-AAB levels lower than < 2 beats/min. Using this cutoff point, patient groups showed significant percentage of β2-AABs (69% OHT, p<0.001; 78% POAG, p<0.001). β2-AAB levels revealed no significant differences (Kruskal-Wallis-test: p>0.05) between OHT (5.23±1.94) and POAG (5.15±1.20). Subgroup analysis for glaucoma patients with and without perimetric defects showed no significant differences in the percentage of β2-AAB positivity (83% pre-POAG, 78% POAG) and the levels of β2-AABs (pre-POAG 5.61±1.13, POAG 4.87±1.19).
Conclusions:
The high percentage of β2-AAB positivity in glaucoma patients suggests a potential role for β2-AAB in glaucoma disease. The same percentage of β2-AAB positivity and the β2-AAB levels in OHTs, early and late glaucoma might indicate a primary role for β2-AAB in glaucoma pathophysiology. (1) Dragun D et al. (2005) Angiotensin II type 1-receptor activating antibodies in renal-allograft rejection. N Engl J Med 352: 558-569
Keywords: 432 autoimmune disease •
447 cell-cell communication