The JI PBL Intereron Source
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     
 

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
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
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Zoda, T.
Right arrow Articles by Krolick, K. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zoda, T.
Right arrow Articles by Krolick, K. A.

The Journal of Immunology, Vol 146, Issue 2 663-670, Copyright © 1991 by American Association of Immunologists

ARTICLES

Clonotypic analysis of anti-acetylcholine receptor antibodies from experimental autoimmune myasthenia gravis-sensitive Lewis rats and experimental autoimmune myasthenia gravis-resistant Wistar Furth rats

T Zoda, TM Yeh and KA Krolick
Department of Microbiology, University of Texas Health Science Center, San Antonio 78284.

A single immunization of Lewis rats with purified acetylcholine receptor (AChR) emulsified in adjuvant typically stimulates the production of oligoclonal AChR-reactive antibodies (as demonstrated by IEF) dominated by the IgG2a subclass, of moderate but clonotypically heterogeneous relative Ag-binding avidity, and capable of inducing symptoms of experimental autoimmune myasthenia gravis. Although similar immunization of Wistar Furth rats produces AChR-reactive antibodies with similar characteristics of clonotypic heterogeneity, avidity, and isotype expression, no detectable signs of AChR-dependent muscle impairment is observed. This contrasts the ability to induce impaired AChR function upon the passive transfer of pre-formed Lewis anti-AChR antibodies into naive Wistar Furth rats, suggesting that disease resistance in this model is not conferred at the level of the AChR itself. Moreover, if more aggressive immunization protocols are used (i.e., multiple injections of AChR), a transient breakthrough of AChR- dependent muscle dysfunction can be induced directly in the Wistar Furth strain indicating that the potential for the production of disease-causing antibodies does exist in the Wistar Furth repertoire. IEF analysis of Wistar Furth anti-AChR antibodies has revealed that hyperimmunization results in modified antibody clonotype expression that might explain changing expression of disease symptoms; however, explanations for the apparent "resistance" of Wistar Furth rats to disease induction are likely to be complex.


This article has been cited by other articles:


Home page
 NeurologyHome page
A. C. Vincent, J. McConville, J. Newsom-Davis, J. M. Lindstrom, and A. G. Engel
Is "seronegative" MG explained by autoantibodies to MuSK?
Neurology, January 25, 2005; 64(2): 399 - 399.
[Full Text] [PDF]

Home page
 Infect. Immun.Home page
P. S. Rajapakse, N. M. O'Brien-Simpson, N. Slakeski, B. Hoffmann, and E. C. Reynolds
Immunization with the RgpA-Kgp Proteinase-Adhesin Complexes of Porphyromonas gingivalis Protects against Periodontal Bone Loss in the Rat Periodontitis Model
Infect. Immun., May 1, 2002; 70(5): 2480 - 2486.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
A. Saoudi, I. Bernard, A. Hoedemaekers, B. Cautain, K. Martinez, P. Druet, M. De Baets, and J.-C. Guery
Experimental Autoimmune Myasthenia Gravis May Occur in the Context of a Polarized Th1- or Th2-Type Immune Response in Rats
J. Immunol., June 15, 1999; 162(12): 7189 - 7197.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 1991 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 1991 by The American Association of Immunologists, Inc. All rights reserved.