CONCEPT OF AUTOIMMUNITY FOLLOWING SPINAL-CORD INJURY - POSSIBLE ROLESFOR T-LYMPHOCYTES IN THE TRAUMATIZED CENTRAL-NERVOUS-SYSTEM

The effect of immunological activation on the neuropathologic sequelae and neurologic outcome from spinal cord injury is unclear, Similar to models of neuroinflammatory disease (e.g., experimental autoimmune en cephalomyelitis; EAE), injury to the spinal cord precipitates the acti vation of resident micro glia and the recruitment of circulating infla mmatory cells (e.g., macrophages and lymphocytes), In EAE, these cells are known to cause tissue damage and loss of neurological function vi a autoimmune reactions to myelin proteins, The role these cells play i n the pathology of traumatic injury to the spinal cord has not been cl arified, In this review, data are presented that indicate that T cells isolated from spinal-injured rats are capable of causing neurologic d eficits and histopathologic changes similar to EAE when injected intra venously into naive animals. These data are consistent with the concep t of trauma-induced autoimmune reactions, However, disease transfer wa s only possible when T cells were obtained from animals at 1 week post -injury, Thus, the encephalitogenic T-cell repertoire appears to be ra pidly regulated, It is possible that trauma-induced autoimmunity evolv es into a mechanism by which the autoreactive repertoire regulates ong oing central nervous system (CNS) immunologic responses, Similar immun oregulatory networks have been proposed in EAE and are discussed here in the context of CNS trauma and neurodegenerative disease. (C) 1996 W iley-Liss, Inc.