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Interferon-beta (IFNβ) treatment represents a major advance in the management of MS that was made without a complete understanding of the cause of MS or the mechanism of action of IFNβ. It is widely believed that MS is an immune-mediated disease and that the mechanism of action of IFNβ is related to its immunomodulatory activity. In December 1996, two articles1,2 and an editorial3 were published that proposed, based on in vitro studies, that the therapeutic effect of IFNβ in MS might be caused by an inhibition of matrix metalloproteinase-9 (92-kDa type IV collagenase or MMP-9). Transmigration of activated lymphocytes across basement membranes is dependent on secreted MMP-9, and the two studies showed that IFNβ decreased MMP-9 secretion and lymphocyte transmigration across an artificial basement membrane. It was proposed that IFNβ treatment blocked lesion formation in MS by limiting the entry of lymphocytes into the CNS. If this hypothesis is true, then lymphocytic-secreted MMP-9 activity should increase before the appearance of new lesions and secreted MMP-9 activity should decrease during treatment with IFNβ in MS patients. This issue of Neurology contains two articles examining these questions in patients with MS, specifically following serum levels of MMP-9. Both provide data that support the hypothesis. Waubant …
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