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Pathogenesis of myelin/oligodendrocyte damage in multiple sclerosis

From the Department of Neurology, University of Medicine and Dentistry of New Jersey–Robert Wood Johnson Medical School, New Brunswick, New Jersey.

Address correspondence and reprint requests to Dr. Suhayl Dhib-Jalbut, Department of Neurology, University of Medicine and Dentistry of New Jersey–Robert Wood Johnson Medical School, 97 Patterson St, New Brunswick, NJ 08901-2160 jalbutsu{at}umdnj.edu

Substantial evidence supports autoimmune activity as the etiologic mechanism underlying multiple sclerosis (MS). Both the innate and the adaptive arms of the immune system are involved in the aberrant response to several antigens associated with the myelin sheath and oligodendrocytes (OGCs) after the activation of immune cells by self- or cross-reactive microbial pathogens. The CD4⁺ Th1 cell, in particular, has been implicated, but it is abetted by a variety of other cell types (CD8⁺ cells, B cells, macrophages, and microglia) and soluble products (proteases, cytokines, and nitric oxide [NO]) that act both outside of and within the CNS. This review describes recent and salient findings from animal models and human clinical studies that have established our current understanding of the distinct steps in the development of immune autoreactivity that culminates in the CNS lesions associated with MS.

This supplement was supported by an educational grant from Teva Neuroscience. BioScience Communications contributed to the editorial refinement of this article and to the production of this supplement. Authors may have accepted honoraria for their supplement contributions.

Disclosure: S.D.J. has received research grants from TEVA Pharmaceuticals. He has been a member of the Speakers' Bureau of and a Consultant to TEVA Pharmaceuticals, Berlex, and Serono.

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represents the opinions of the authors and is not endorsed by nor does it reflect the views of the American Academy of Neurology, Editorial Board, Editor-in-Chief, or Associate Editors of Neurology.