The gut-retina axis: Uncovering the role of autoimmunity in glaucoma development

Abstract

Glaucoma, a leading cause of irreversible blindness worldwide, is characterized by progressive loss of retinal ganglion cells (RGCs) and optic nerve damage. While elevated intraocular pressure (IOP) is the only known modifiable risk factor, normal-tension glaucoma (NTG) challenges this notion, suggesting other mechanisms beyond IOP may contribute to its development. Emerging evidence support the hypothesis that glaucoma may be an autoimmune disease. This review summarizes evidence for this hypothesis, focusing on the gut-retina axis. We discuss how antigens of gut bacterial prime peripheral T cells to breach the blood-retina barrier (BRB) and initiate cross-reactivity with ocular tissues via molecular mimicry, resulting in autoimmune RGC damage. Understanding these mechanisms may uncover new diagnostic biomarkers and therapeutic strategies targeting immune pathways alongside conventional IOP-lowering treatments.

Keywords

• Glaucoma
• Autoimmunity
• Gut-retina axis
• T cell
• Heat shock proteins (HSPs)