Purpose of review: Compelling evidence obtained from studies over the last decade strongly suggests the involvement of immune system regulation in cell fate decisions in glia and retinal ganglion cells that lead to glaucomatous optic nerve degeneration.
Recent findings: Recent studies reveal seemingly conflicting roles of the immune system in glaucomatous optic nerve degeneration. T cells directed against specific antigens may have a beneficial effect to protect neurons from the consequences of axonal injury. However, the immune response in glaucoma also has the capacity to cause neuronal injury. The balance between the benefit of protective immunity and the risk of inducing an autoimmune neurodegenerative disease is critical. The immunoregulatory function of glial cells and the presence of tissue stress seem to be important factors that determine the balance between diverse roles of the immune system in glaucomatous optic nerve degeneration. Thus, the net effect of immunoregulation may be either neuroprotective or neurodestructive.
Summary: Despite the neuroprotective features of the immune system, an autoimmune component, resulting from a failure to properly control aberrant, stress-induced immune response, likely accompanies the progression of neurodegeneration in glaucoma in some patients. A better understanding of the diverse roles of the immune system in all forms of glaucomatous optic nerve degeneration will facilitate the development of effective neuroprotective strategies in glaucoma. The basis of a sustainable neuroprotective strategy is to harness immunoregulation of glial and retinal ganglion cell fate to maximize beneficial effects, while minimizing negative sequelae, for therapeutic gain.