Immune regulation toward immunomodulation for neuroprotection in glaucoma

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.

► Immune system is activated in human glaucoma and experimental models. ► Glia play key roles in innate immune responses and the innate/adaptive interplay. ► Cytokines, TLRs, NF-κB, inflammasome, and complement are co-players. ► Homeostasis of immune response pathways determines the neurodegenerative potential. ► Immunomodulation may serve as a neuroprotective treatment strategy.