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


     
 

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
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 Reyes-Reyna, S.
Right arrow Articles by Krolick, K. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Reyes-Reyna, S.
Right arrow Articles by Krolick, K. A.
The Journal of Immunology, 2002, 169: 1579-1586.
Copyright © 2002 by The American Association of Immunologists

Muscle Responds to an Antibody Reactive with the Acetylcholine Receptor by Up-Regulating Monocyte Chemoattractant Protein 1: A Chemokine with the Potential to Influence the Severity and Course of Experimental Myasthenia Gravis1

Sara Reyes-Reyna, Timothy Stegall and Keith A. Krolick2

Department of Microbiology, University of Texas Health Science Center, San Antonio, TX 78229

Autoantibodies with reactivity against the postjunctional muscle receptor for acetylcholine receptor are able to interfere with contractile function of skeletal muscles and cause the symptoms of myasthenia gravis (MG) in humans, as well as in experimental animal models of MG. In the study described below using a rat model of MG, it was observed that exposure to acetylcholine receptor-reactive Abs also induced increased levels of chemokine (i.e., monocyte chemoattractant protein 1) production by skeletal muscle cells. This was true of both cultured rat myocytes exposed in vitro and rat muscle exposed in vivo following passive Ab transfer. Increased monocyte chemoattractant protein 1 production may explain the increased trafficking of leukocytes through muscle following Ab transfer described in this and other reports. These observations may also be relevant to the induction of disease symptoms in experimental animal models of MG, since numerous reports from this and other laboratories indicate that the cytokine environment provided by leukocytes trafficking through muscle may play a pivotal role in disease progression.




This article has been cited by other articles:


Home page
 J. Physiol.Home page
L. Yahiaoui, D. Gvozdic, G. Danialou, M. Mack, and B. J. Petrof
CC family chemokines directly regulate myoblast responses to skeletal muscle injury
J. Physiol., August 15, 2008; 586(16): 3991 - 4004.
[Abstract] [Full Text] [PDF]

Home page
 J. Leukoc. Biol.Home page
G. Gatti, V. Rivero, R. D. Motrich, and M. Maccioni
Prostate epithelial cells can act as early sensors of infection by up-regulating TLR4 expression and proinflammatory mediators upon LPS stimulation
J. Leukoc. Biol., May 1, 2006; 79(5): 989 - 998.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
T. Feferman, P. K. Maiti, S. Berrih-Aknin, J. Bismuth, J. Bidault, S. Fuchs, and M. C. Souroujon
Overexpression of IFN-Induced Protein 10 and Its Receptor CXCR3 in Myasthenia Gravis
J. Immunol., May 1, 2005; 174(9): 5324 - 5331.
[Abstract] [Full Text] [PDF]

Home page
 J. Immunol.Home page
J. Pritchard, S. Tsui, N. Horst, W. W. Cruikshank, and T. J. Smith
Synovial Fibroblasts from Patients with Rheumatoid Arthritis, Like Fibroblasts from Graves' Disease, Express High Levels of IL-16 When Treated with Igs against Insulin-Like Growth Factor-1 Receptor
J. Immunol., September 1, 2004; 173(5): 3564 - 3569.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Website Copyright © 2002 by The American Association of Immunologists, Inc. All rights reserved.
All Contents Copyright © 2002 by The American Association of Immunologists, Inc. All rights reserved.