Immune regulation toward immunomodulation for neuroprotection in glaucoma

Abstract

Although the immune system functions to preserve and restore tissue homeostasis, accumulating risk factors, prolonged glial activation, and sustained release of pro-inflammatory mediators in glaucoma may lead to a failure in the regulation of stress-induced immune response, and innate immune cells, autoreactive T cells, autoantibodies, and excess complement attack may exhibit potent stimuli that harm retinal ganglion cell somas, axons, and synapses. Identification of the cellular and molecular components of immune response pathways can provide immunomodulatory treatment strategies to attenuate neuroinflammation, protect neural tissue from collateral injury, and enhance endogenous recovery processes. This review highlights the current knowledge of molecular mechanisms regulating neuroinflammation in glaucoma.

Figure 1

Immune regulation in glaucoma. Various pathways, such as pro-inflammatory cytokine signaling (including TNF-α/TNFR signaling), TLR signaling, NF-κB activation, NLRs and inflammasome assembly, and complement activation are co-players of inflammatory responses in glaucomatous tissues. A failure in the regulation of immune response pathways may shift the physiological equilibrium toward an inflammatory neurodegenerative process.