Purpose   Myelin basic protein (MBP) is the key protein, which induces the pathogenesis of experimental autoimmune encephalomyelitis (EAE) by attacking the central nerve system neurons though activated the specific T-cells. The aim of our study was to examine the effects of myelin basic protein (MBP) immunization on the survival of optic never axon and retina ganglion cells (RGCs) in the acute retina ischemia mice model.

Methods    immunized mice with MBP combined with Incomplete Freund’s Adjuvant（IFA）. The mice immunized by ovalbumin (OVA) combined with IFA were used as control group. The reactions of T cell were detected by Elispot after 2 weeks of immunization. All the mice were induce the acute retina ischemia in mice by elevated the intraocular pressure (IOP) up to 100mmHg to 1 hour after immunized with antigen for 2 weeks.  Optic nerve axon and RGCs density was evaluated by optic nerve EM section and immunostaining on retinal flat mounts. T cell infiltration, IgG antibody deposition and cytokines were examined in retina and optic nerve sections. The intensity of autoreactive IgG antibodies was quantified in serum, and cytokines released in the draining lymph node were examined by flowcytometry.

Results   the RGCs density in the EAE ischemia mice group were 2171±227（neurons／mm²），and the OVA control group were 1838±128 （neurons／mm²). Significant loss of optic nerve axon and RGCs were detected in the EAE ischemia mice group compare to the OVA control group (p < 0.05). At the same time, IgG antibody deposits accumulated in the retina of EAE ischemia mice group. The level of IgG antibody reactivity against retina and optic nerve tissue continuously increased (p < 0.05).  The release of IFN-γ, IL-1, TNF-a, IL-17, Vimentin and GFAP were highly up regulated compare to the control group.

Results  Immunization with MBP can causes neuron and axon loss in the retinal ganglion cell layer and optic nerve by triggering T cell mediated immune response. And antibody reactivity against ocular tissue might also involve in the pathogenesis. This study suggests that, T-cell mediation and antibody reactivity both influence the ocular path mechanisms in the EAE ischemia mice model.