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From the Departments of Oncology and Clinical Neurosciences (Dr. Yong and S. Chabot), Faculty of Medicine, University of Calgary, Alberta, Canada; the Department of Neurology (Dr. Stuve), University of Washington, Seattle, WA; and Berlex Laboratories (Dr. Williams), Richmond, CA.
Address correspondence and reprint requests to Dr. V. Wee Yong, Neuroscience Research Group, Departments of Oncology and Clinical Neurosciences, 3330 Hospital Drive NW, Calgary, Alberta T2N 4N1 Canada.
Interferon beta (IFN-ß) has been shown in several clinical trials to have efficacy in MS. Its mechanism of action, however, remains unclear. In this review, several biological activities of IFN-ß are highlighted, including its inhibitory effects on proliferation of leukocytes and antigen presentation. Furthermore, IFN-ß may modulate the profile of cytokine production toward that of the anti-inflammatory phenotype, and this appears to occur in the systemic circulation and within the CNS. Finally, IFN-ß can reduce T-cell migration by inhibiting the activity of T-cell matrix metalloproteinases. These activities are likely to act in concert to account for the mechanism of IFN-ß in MS.
Supported by Berlex Laboratories, Richmond, CA and Medical Services Incorporated, Alberta, Canada.
Received March 3, 1998. Accepted in final form May 20, 1998.
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