RT Journal Article SR Electronic T1 Vaccination for Neuroprotection in the Mouse Optic Nerve: Implications for Optic Neuropathies JF The Journal of Neuroscience JO J. Neurosci. FD Society for Neuroscience SP 136 OP 142 DO 10.1523/JNEUROSCI.21-01-00136.2001 VO 21 IS 1 A1 Jasmin Fisher A1 Hanna Levkovitch-Verbin A1 Hadas Schori A1 Eti Yoles A1 Oleg Butovsky A1 Joel F. Kaye A1 Avraham Ben-Nun A1 Michal Schwartz YR 2001 UL http://www.jneurosci.org/content/21/1/136.abstract AB T-cell autoimmunity to myelin basic protein was recently shown to be neuroprotective in injured rat optic nerves. In the present study, using the mouse optic nerve, we examined whether active immunization rather than passive transfer of T-cells can be beneficial in protecting retinal ganglion cells (RGCs) from post-traumatic death. Before severe crush injury of the optic nerve, SJL/J and C3H.SW mice were actively immunized with encephalitogenic or nonencephalitogenic peptides of proteolipid protein (PLP) or myelin oligodendrocyte glycoprotein (MOG), respectively. At different times after the injury, the numbers of surviving RGCs in both strains immunized with the nonencephalitogenic peptides pPLP 190–209 or pMOG 1–22 were significantly higher than in injured controls treated with the non-self-antigen ovalbumin or with a peptide derived from β-amyloid, a non-myelin-associated protein. Immunization with the encephalitogenic myelin peptide pPLP 139–151 was beneficial only when the disease it induced, experimental autoimmune encephalomyelitis, was mild. The results of this study show that survival of RGCs after axonal injury can be enhanced by vaccination with an appropriate self-antigen. Furthermore, the use of nonencephalitogenic myelin peptides for immunization apparently allows neuroprotection without incurring the risk of an autoimmune disease. Application of these findings might lead to a promising new approach for treating optic neuropathies such as glaucoma.