Neurology 2002;58:S3-S9
© 2002 American Academy of Neurology
| Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology.
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Mechanisms of action of interferons and glatiramer acetate in multiple sclerosis
Suhayl Dhib-Jalbut, MD
From the Department of Neurology, University of Maryland School of Medicine, and the Baltimore VA Medical Center, Baltimore, MD.
Address correspondence and reprint requests to: Dr. Suhayl Dhib-Jalbut, Department of Neurology, University of Maryland Hospital, 22 S. Greene St., Rm. N4W46, Baltimore, MD 21201.
MS is an immunologically mediated disease, as determined by observation of the response to immunotherapy and the existence of an animal model, experimental autoimmune encephalitis. Interferon (IFN) ß-1b, IFN ß-1a, and glatiramer acetate, the therapies used for relapsing or remitting MS, have mechanisms of action that address the immunologic pathophysiology of MS. The IFNs bind to cell surface-specific receptors, initiating a cascade of signaling pathways that end with the secretion of antiviral, antiproliferative, and immunomodulatory gene products. Glatiramer acetate, a synthetic molecule, inhibits the activation of myelin basic protein-reactive T cells and induces a T-cell repertoire characterized by anti-inflammatory effects. Although the two classes of drugs have some overlapping mechanisms of action, the IFNs rapidly block blood–brain barrier leakage and gadolinium (Gd) enhancement within 2 weeks, whereas glatiramer acetate produces less rapid resolution of Gd-enhanced MRI activity. IFN ß has no direct effects in the CNS, but glatiramer acetate-specific T cells are believed to have access to the CNS, where they can exert anti-inflammatory and possibly neuroprotective effects.
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