Abstract :
The primary caue of neurodegeneration in glaucoma ha not been identified. At any given time the affected optic nerve contain fiber that are amenable to neuroprotection, and will ecape degeneration provided that the proper pharmacological or other intervention i applied. Autoimmunity ha long been viewed a a deleteriou phenomenon that hould be terminated or at leat minimized in order to preerve health. The author recently demontrated that T cell pecific to elf-protein reiding in the ite of CNinult can be protective. With the aim of booting autoimmunity for neuroprotection without riking the induction of an autoimmune dieae, the ue of Cop-1 (an FDA-approved drug for the treatment of multiple cleroi) a an active vaccination for neuroprotection ha been developed. Cop-1 i a ynthetic polymer that weakly cro-react with a wide range of elf-reacting T cell. Vaccination with Cop-1 reulted in ignificant neuroprotection in rat model of optic nerve cruh and chronic glaucoma. Thu, booting of a T cell-baed mechanim, which ha been termed “protective autoimmunity”, promote recovery of the damaged optic nerve. Current tudie are aimed at tranlating thi treatment into a clinical therapy.—Han E. Groniklau
