Abstract: Investigation into mechanisms that are independent of IOP, but cause initial or secondary damages to retinal ganglion cells and/or their axons is imperative. The retina is a part of the central nervous system (CNS). POAG and other neurodegenerative diseases may share some common pathological mechanisms, of which the neuroimmunity-inflammation plays a pivotal role. State-of-the-art findings on immune mechanisms of CNS neurodegeneration may shed some novel insight into the exploration of POAG pathogenesis. From a perspective of neuroscience and immunology, focusing on microglia and T lymphocytes in light of the latest findings in immune mechanisms of neurodegeneration, we have therefore established a novel theoretical structure integrating existing knowledge on the pathogenesis of POAG. Altogether, we speculate that mechanisms of POAG immune injury is as follows: neuron damage-associated antigens activate microglia releasing pro-inflammatory factors and increasing the adhesion of peripheral circulating leukocytes, and thereafter the permeability of BRB changes; the antigen presentation process may be achieved through diverse pathways; in lymphoid organs, T cells clone, proliferate and differentiate induced by the interaction with APCs, and then antigen-specific T cells enter the retina through the BRB, causing the exacerbation of immune-inflammatory damage to retinal neurons. (Ophthalmol CHN, 2021, 30: 5-10)

Key words: primary open angle glaucoma, blood retinal barrier, microglia, immunity