Role of T cell-induced autoimmune response in the pathogenesis of glaucoma

This review aims to elucidate the role of T cell-induced autoimmune responses in the pathogenesis of glaucoma, focusing on the immunological changes contributing to retinal ganglion cell (RGC) damage.

A comprehensive review of recent studies examining immunological mechanisms in glaucoma was conducted. This included analyses of T cell interactions, heat shock proteins (HSPs), and resultant autoimmune responses. Key findings from experimental models and clinical observations were synthesized to present a coherent understanding of immune dynamics in glaucoma.

Glaucoma is a neurodegenerative disease marked by optic nerve atrophy and irreversible vision loss due to RGC damage. The disease is etiologically heterogeneous, with multiple risk factors and pathogenic mechanisms. Recent research highlights the dual immunomodulatory role of T cells in immune protection and injury. T cells, pre-sensitized by bacterial HSPs, can cross-react with endogenous HSPs in RGCs under stress, leading to autoimmune damage. Elevated levels of HSP autoantibodies and abnormal T cell activity have been observed in glaucoma patients, indicating a significant autoimmune component in disease progression.

T cell-induced autoimmune responses are crucial in the pathogenesis of glaucoma, contributing to RGC degeneration beyond the effects of elevated intraocular pressure. Understanding these immunological mechanisms is vital for developing targeted neuroprotective therapies for glaucoma.