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  Vol. 63 No. 10, October 2006 TABLE OF CONTENTS
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Natalizumab and Immune Cells

Arch Neurol. 2006;63:1366-1367.

Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Understanding the mechanisms underlying the unfortunate occurrence of progressive multifocal leukoencephalopathy (PML), a disease caused by reactivation of the JC polyomavirus, in a small subset of patients during treatment of autoimmune disease with natalizumab is important at several levels. The most important and immediate outcome would be a more complete appreciation of the risk of PML, not only with natalizumab therapy but also with other immunomodulatory therapeutic strategies currently in development. The second most important outcome would be the potential for the development of approaches for monitoring patients treated with natalizumab and other therapies that may have similar risks, in turn allowing for the safer use of these treatments. Finally, an understanding of the mechanism(s) contributing to the association of PML with natalizumab therapy may provide new insights into the disease processes in multiple sclerosis and PML.

Two general mechanisms have been suggested to explain the association between natalizumab treatment . . . [Full Text of this Article]

AUTHOR INFORMATION

Henry F. McFarland, MD; Steven Jacobson, PhD



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RELATED ARTICLE

Altered CD4+/CD8+ T-Cell Ratios in Cerebrospinal Fluid of Natalizumab-Treated Patients With Multiple Sclerosis
Olaf Stüve, Christina M. Marra, Amit Bar-Or, Masaaki Niino, Petra D. Cravens, Sabine Cepok, Elliot M. Frohman, J. Theodore Phillips, Gabriele Arendt, Keith R. Jerome, Linda Cook, Francois Grand'Maison, Bernhard Hemmer, Nancy L. Monson, and Michael K. Racke
Arch Neurol. 2006;63(10):1383-1387.
ABSTRACT | FULL TEXT  






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