More MS news articles for Nov 2001

Immunopathology of secondary-progressive multiple sclerosis

http://www3.interscience.wiley.com/cgi-bin/abstract/85514733/START
 

Annals of Neurology
Volume 50, Issue 5, 2001. Pages: 646-657
Published Online: 5 Oct 2001
John W. Prineas, MB, BS (1) *, Eunice E. Kwon, MSc (2), Eun-Sook Cho, MD (2), Leroy R. Sharer, MD (2), Michael H. Barnett, MB, BS (1), Emilia L. Oleszak, PhD (3), Brad Hoffman, BS (3), Bryan P. Morgan, PhD (4)
1 Department of Medicine, University of Sydney, NSW, Australia
2 Departments of Neuroscience and Pathology, University of Medicine and Dentistry of New Jersey, New Jersey Medical School, Newark the Veterans' Administration Medical Center, East Orange, NJ
3 Fels Institute and Temple University School of Medicine, Philadelphia, PA
4 Department of Medical Biochemistry, University of Wales College of Medicine, Cardiff, UK
 email: John W. Prineas (larapinta@bigpond.com)
*Correspondence to John W. Prineas, Department of Medicine, Blackburn Building, University of Sydney, NSW 2006 Australia

Abstract

Twenty-three plaques obtained at early autopsy from 2 patients with secondary-progressive multiple sclerosis were examined immunohistochemically for microglia/macrophages, and for immunoglobulins and components of activated complement.

Most of the lesions examined in both cases exhibited evidence of low-grade active demyelination of an unusual type (frustrated phagocytosis) in periplaque white matter.

This included linear groups of microglia engaging short segments of disrupted myelin that were associated with deposits of C3d, an opsonin formed during complement activation.

Similar microglia/C3d/myelin profiles were not observed in newly forming lesions in cases of acute multiple sclerosis or other central white matter diseases.

As C3d coupling is known to increase the immunogenicity of potential antigens enormously, present findings point to disrupted myelin close to plaques as a possible source of the putative multiple sclerosis antigen.

Ongoing myelin destruction found in a high proportion of old, established plaques was surprising.

It suggests that slowly expanding lesions (progressive plaques), in which ongoing myelin breakdown occurs in the absence of florid perivascular cell cuffing or other histological signs of acute inflammation, contribute to disease progression in cases of secondary-progressive multiple sclerosis.

Funded by:

Medical Research Service of the Department of Veteran Affairs
National Multiple Sclerosis Society
 

Copyright © 2001 Wiley-Liss, Inc