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From the Department of Neurology, Medical Academy of Lodz, Poland (Dr. Selmaj), and the Department of Pathology, Albert Einstein College of Medicine, Bronx, N.Y. (Drs. Selmaj and Raine).
Address correspondence and reprint requests to Professor K. Selmaj, Department of Neurology, Medical Academy of Lodz, 22 Kopcinskiego Street, 90-153 Lodz, Poland.
Multiple sclerosis (MS) is a demyelinating disease in which an inflammatory cell infiltrate represents a characteristic pathologic feature of active lesions within the CNS.The possibility has been raised that cell-mediated immune mechanisms orchestrate the pathogenesis of MS. Cytokines play a particularly important role in cellular immune mechanisms. These soluble glycoproteins, nonimmunoglobulin in nature, act nonenzymatically to regulate immune cell function. A unique family of cytokines, the tumor necrosis factors (TNFs), demonstrate immunoregulatory activity but are also involved in the effector arm of cellular immune responses. Recently, studies both in vitro and in vivo have suggested a role for TNFs in the pathology of MS. This report summarizes data implicating TNFs in the mechanisms of MS and attempts to apply the anti-TNF approach in the future therapeutic strategy for this disease.
NEUROLOGY 1995;45(Suppl 6): S44-S49
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