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Antibody to myelin-associated glycoprotein produces central nervous system demyelination

From the Departments of Neurology (Drs. Sergott, Brown, and Lisak) and Ophthalmology (Dr. Sergott), University of Pennsylvania School of Medicine, and the Wistar Institute (Dr. Miller), Philadelphia, PA.

Antibodies to myelin-associated glycoprotein (MAG) have been implicated in certain human demyelinating diseases of the peripheral nervous system. In the present study, a monoclonal antibody to MAG with 20% guinea pig serum (GPS) was injected into mammalian optic nerves and produced in vivo demyelination associated with three ultrastructural patterns of myelin injury: (1) widened lamellae; (2) myelin vesiculation; and (3) cell-associated myelin damage. These patterns of myelin injury have been observed neuropathologically in MS and in a demyelinating peripheral neuropathy associated with plasma cell dyscrasias. Demyelination was not observed in nerves injected with anti-MAG and heated GPS or a monoclonal antibody to chick myoblasts and 20% GPS. These results establish the ability of anti-MAG to produce in vivo demyelination of mammalian CNS and indicate that a single antibody directed against a specific myelin component may initiate multiple types of myelin damage.

Address correspondence and reprint requests to Dr. Sergott, University of Pennsylvania School of Medicine, Department of Neurology, 3400 Spruce Street, Philadelphia. PA 19104.

Supported by United States Public Health Service grants NS11037 and NS08075 and a grant from the National Multiple Sclerosis Society. Presented in part at the thirty-seventh annual meeting of the American Academy of Neurology, Dallas, TX, May 1985.

Received February 5, 1987. Accepted for publication in final form June 9, 1987.

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