The T lymphocyte in experimental allergic encephalomyelitis

SS Zamvil, L Steinman - Annual review of immunology, 1990 - annualreviews.org
Annual review of immunology, 1990annualreviews.org
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. Experi mental allergic encephalomyelitis (EAE) is a prototype for antigen-specific T
cell-mediated autoimmune disease (1, 2). The auto antigen in EAE is myelin basic protein
(MBP), the predominant protein of central nervous system myelin. EAE is mediated by class …
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. Experi mental allergic encephalomyelitis (EAE) is a prototype for antigen-specific T cell-mediated autoimmune disease (1, 2). The auto antigen in EAE is 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 ofEAE are characterized by relaps ing paralysis, with histopathology demonstrating perivascular lymphocytic infiltrates and demyelination within the central nervous system (eNS). Because of these and other clinical and histologic features, relapsing EAE is considered as a model for the human demyelinating disease multiple sclerosis (MS)(3, 4). Furthermore, susceptibility for both EAE and MS (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 579
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