help button home button Am J Pathol R & D Systems
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Burrer, R.
Right arrow Articles by von Herrath, M. G.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Burrer, R.
Right arrow Articles by von Herrath, M. G.
(American Journal of Pathology. 2007;170:557-566.)
© 2007 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2007.060893

Exacerbated Pathology of Viral Encephalitis in Mice with Central Nervous System-Specific Autoantibodies

Renaud Burrer*, Michael J. Buchmeier*, Tom Wolfe{dagger}, Joey P.C. Ting*, Ralph Feuer*, Antonio Iglesias{ddagger} and Matthias G. von Herrath{dagger}

From the Molecular and Integrative Neurosciences Department,* The Scripps Research Institute, La Jolla, California; the La Jolla Institute of Allergy and Immunology,{dagger} Immune Regulation Lab, La Jolla, California; and the Roche Center for Medical Genomics,{ddagger} Basel, Switzerland

We examine here the outcome of viral encephalomyelitis [mouse hepatitis virus (MHV) A59, Theiler’s encephalomyelitis virus, and Coxsackievirus B3] in mice with autoantibodies to a central nervous system (CNS)-specific antigen, myelin oligodendrocyte glycoprotein, that usually develop no clinical disease. Morbidity and mortality of the acute viral CNS disease was augmented by the presence of the autoantibodies in all three viral infections. Transfer of serum containing the autoantibodies at the time of infection with MHV was sufficient to reproduce the exacerbated disease. The presence of the autoantibodies was found to result in increased infiltration of mononuclear cells into the brain. Early demyelination was severely augmented in brains and spinal cords of MHV-infected mice with CNS-specific autoantibodies. The antibody-mediated exacerbation was shown to be independent of the complement system but to require expression of Fc receptors, because it was observed in C'-3-deficient but not in Fc receptor-deficient mice. Our study illustrates the possibility that infections can lead to much more profound immunopathology in the presence of an otherwise latent autoimmune condition.




This article has been cited by other articles:


Home page
 Mult SclerHome page
S. Amor and G. Giovannoni
Antibodies to myelin oligodendrocyte glycoprotein as a biomarker in multiple sclerosis are we there yet?
Multiple Sclerosis, November 1, 2007; 13(9): 1083 - 1085.
[PDF]

Home page
 Am. J. Pathol.Home page
R. A. Sobel
Anti-Viral T-Cell Immunity + Anti-CNS Autoantibody = A Model for Human Acute Disseminated Encephalomyelitis or Multiple Sclerosis Relapse?
Am. J. Pathol., February 1, 2007; 170(2): 436 - 438.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2007 by the American Society for Investigative Pathology.