View article

Discrimination between foreign and self antigens is necessary for normal immune function. Whereas exposure to foreign antigens can lead to their elimination and subsequent specific immunity, an unregulated immune response to self antigens may culminate in autoimmune disease. Experimental allergic encephalomyelitis (EAE) is a prototype for antigen-specific T cell-mediated autoimmune disease (l, 2). The autoantigen in EAE myelin basic protein (MBP), the predominant protein of central nervous system myelin. EAE is mediated by class II-restricted, MBP-specific CD4+ T lymphocytes. Certain forms of EAE are characterized by relapsing paralysis, with histopathology demonstrating perivascular lymphocytic infiltrates and demyelination within the central nervous system (CNS). Because of these and other clinical and histologic features, relapsing EAE is considered as a model for the human demyelinating disease multiple scleros& (MS)(3, 4). Furthermore, susceptibility for both EAE and (5) is linked to class-II (immune response) genes. As a model for human autoimmune disease, EAE has been useful for testing novel forms of immunotherapy. A major goal for such testing is to develop modalities that can selectively inactivate or eliminate only those cells involved in disease pathogenesis. Several studies have demonstrated that antibodies targeted at class-II molecules, CD4, and T cell receptor