A monoclonal antibody against a myelin oligodendrocyte glycoprotein induces relapses and demyelination in central nervous system autoimmune disease.

HJ Schluesener, RA Sobel, C Linington… - Journal of immunology …, 1987 - journals.aai.org
HJ Schluesener, RA Sobel, C Linington, HL Weiner
Journal of immunology (Baltimore, Md.: 1950), 1987journals.aai.org
The factors contributing to chronic relapsing inflammatory disease processes of the central
nervous system (CNS) and demyelination are poorly understood. In addition to cellular
immune reactions, humoral factors such as antibodies might quantitatively or qualitatively
influence the disease process. We therefore investigated the effects of administration of a
monoclonal antibody specific for a CNS autoantigen on both acute and chronic experimental
autoimmune encephalomyelitis (EAE) in mice and rats. This monoclonal antibody, 8-18C5 …
Abstract
The factors contributing to chronic relapsing inflammatory disease processes of the central nervous system (CNS) and demyelination are poorly understood. In addition to cellular immune reactions, humoral factors such as antibodies might quantitatively or qualitatively influence the disease process. We therefore investigated the effects of administration of a monoclonal antibody specific for a CNS autoantigen on both acute and chronic experimental autoimmune encephalomyelitis (EAE) in mice and rats. This monoclonal antibody, 8-18C5, specific for a myelin/oligodendrocyte glycoprotein, was observed to accelerate clinical and pathologic changes of CNS autoimmune disease. In SJL mice with chronic relapsing EAE, injection of antibody into animals recovering from an attack induced fatal relapses; in Lewis rats, acute EAE was enhanced and associated with a hyperacute inflammatory response with demyelination, a feature not commonly seen in acute EAE. The demonstration that relapses and demyelination can be induced by administration of a white matter-reactive monoclonal antibody offers new possibilities to study processes resulting in CNS damage during autoimmune disease. Furthermore, these findings support the immunopathogenic potential of antibody to myelin components in inflammatory CNS disease processes and, specifically, in causing demyelination.
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