Passive immunization with T cells activated against central nervous system (CNS) - associated myelin antigens has been found to provide neuroprotection following CNS trauma, leading to the concept of protective autoimmunity. However, limited research exists about whether actively induced CNS autoimmunity may offer any similar benefit. In this study, the kinetics and the effect of endogenously anti-myelin activated T cells following spinal cord injury (SCI), were investigated. Experimental allergic encephalomyelitis (EAE) was actively induced in Lewis rats following immunization with myelin basic protein (MBP). In vivo 5-Bromo-2-deoxyuridine (BrdU) incorporation from activated T cells was used as a marker of T cell- proliferation. BrdU was injected on 5th, 6th and 7th day post-induction (DPI) at all EAE-animals. On DPI 8, spinal cord compressive injury was induced by a transient extradural application of an aneurysm clip at the T8 spinal level. SCI resulted in spastic paralysis of hindlimbs, in all but sham-injured animals. Recovery from SCI was significantly better in EAE-animals. Activated mononuclear cells were selectively accumulated at the site of the injury. Axonal loss was less in the EAE group following SCI. Our findings indicate that actively induced autoimmunity against CNS myelin antigens may protect spinal cord pathways from mechanical injury
