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Immunotherapy for Multiple SclerosisThe Curious Case of Interferon Beta
Olaf Stüve, MD, PhD;
Richard M. Ransohoff, MD
Arch Neurol. 2009;66(10):1193-1194.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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Multiple sclerosis (MS) is the most common acquired inflammatory demyelinating disease of the central nervous system in humans. A histopathological hallmark of early MS is the presence of inflammatory cellular infiltrates in actively demyelinating lesions. Most of these cells are macrophages that arise from infiltrating monocytes and microglia and the remaining 10% are T lymphocytes.1 Similar infiltrates cannot be detected in healthy central nervous system tissue. Based on this observation, it has long been considered a therapeutic goal to keep immune-competent cells out of the brains and spinal cords of patients with MS.
In 1993, interferon beta-1b (Betaseron; Bayer HealthCare Pharmaceuticals, Leverkusen, Germany), a recombinant and modified form of human interferon β (IFN-β), was the first agent that was approved for treatment of relapsing-remitting multiple sclerosis. Drug approval was based on the fact that interferon beta-1b therapy reduced the rate of clinical . . . [Full Text of this Article] AUTHOR INFORMATION
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