Glaucoma is a neurodegenerative disease of the optic nerve, which continues to progress even if the primary cause of degeneration is identified and alleviated. At any given time the affected optic nerve contains fibers that are amenable to neuroprotection, and will escape degeneration provided that the proper pharmacological or other intervention is applied. Autoimmunity has long been viewed as a deleterious phenomenon that should be terminated or at least minimized in order to preserve health. We recently demonstrated, however, that T cells specific to self-proteins residing in the site of CNS insult can be protective. With the aim of boosting autoimmunity for neuroprotection without risking the induction of an autoimmune disease, we developed the use of Cop-1 (an FDA-approved drug for the treatment of multiple sclerosis) as an active vaccination for neuroprotection. Cop-1 is a synthetic polymer that weakly cross-reacts with a wide range of self-reacting T cells. Vaccination with Cop-1 resulted in significant neuroprotection in rat models of optic nerve crush and chronic glaucoma. Thus, boosting of a T cell-based mechanism, which we have termed 'protective autoimmunity', promotes recovery of the damaged optic nerve. Current studies in our laboratory are aimed at translating this treatment into a clinical therapy.