Abstract: The term glaucoma encompasses a spectrum of eye diseases pathologically characterized by an irreversible loss of retinal ganglion cells and their associated axons. Patients initially suffer from gaps in their visual field, the part of the visual range that can be perceived without eye movement. In the early stages of the disease, this damage can be compensated very well by eye movements. This, in turn, means that glaucoma is often not diagnosed until the disease is more advanced. However, existing lesions cannot be reversed. High intraocular pressure (IOP) remains one of the main risk factors and the only available therapy is based on its lowering to slow down the progression. It must be emphasized here that there are forms of glaucoma without elevated IOP (normal tension glaucoma) and that the disease continues to progress despite IOP-lowering treatment (Klein et al., 1992). Currently, a cure for glaucoma is not available. The persistent damage to the optic nerve eventually leads to severe visual impairment and even blindness in the patient. This imposes significant limitations on the patient’s independence and quality of life. In addition, it has immense socioeconomic implications. In Western Europe, the annual cost of monthly disability benefits for the blind, staff attrition, and early retirement due to glaucoma is higher than the medical cost of treating the disease. By 2040, Europe is projected to have 7.85 million glaucoma patients (Tham et al., 2014). Therefore, it is of great societal interest to find therapeutic strategies that significantly influence the progression of the disease. A deeper understanding of the underlying pathomechanisms is essential for glaucoma, as they are not fully understood yet. Today, it is already known that various mechanisms contribute to the development of the different forms of glaucoma. Among them, several studies have clearly demonstrated the importance of inflammatory processes in the pathogenesis of glaucoma. For example, differences in systemic as well as ocular antibody profiles were observed in patients suffering from glaucoma (Grus et al., 2004). In addition, antibody depositions were detected in glaucomatous retinae. To further elucidate this, the experimental autoimmune glaucoma (EAG) model was developed. Here, systemic immunization with ocular antigens, such as optic nerve homogenate antigen (ONA) or S100B protein, as part of ONA, leads to optic nerve degeneration and retinal ganglion cell loss (Laspas et al., 2011; Noristani et al., 2016)