|
|
||||||||
The Journal of Immunology, Vol 135, Issue 1 234-241, Copyright © 1985 by American Association of Immunologists
ARTICLES |
CM Gomez and DP Richman
To study the characteristics of the individual autoantibodies that are important in the development of an autoimmune disease, we produced 26 anti-acetylcholine receptor (anti-AChR) monoclonal antibodies (mcAb) and studied the experimental autoimmune myasthenia gravis (EAMG) induced by a number of them. The mcAb reactive with mammalian acetylcholine receptor (M-AChR) exhibited a wide range of dissociation rates from in situ M-AChR of motor endplates. All anti-M-AChR mcAb were capable of producing at least some degree of histopathologic change at the endplate indicative of EAMG, but their potencies varied markedly. One mcAb induced, even at large doses, only minor macrophage invasion without clinical or electromyographic effect. Others induced severe EAMG, and even death, at 1/200th the dose. Low potency was associated with high rate of mcAb dissociation from antigen. High potency was associated with intermediate avidity, not high avidity. These observations suggest that in EAMG, and perhaps in myasthenia gravis, the characteristics of the individual antibodies making up the autoimmune response can determine the severity of the autoimmune disease.
This article has been cited by other articles:
![]() |
C. Amdahl, E. H. Alseth, N. E. Gilhus, H. L. Nakkestad, and G. O. Skeie Polygenic Disease Associations in Thymomatous Myasthenia Gravis Arch Neurol, December 1, 2007; 64(12): 1729 - 1733. [Abstract] [Full Text] [PDF] |
||||
![]() |
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] |
||||
![]() |
B. Balasa, C. Deng, J. Lee, P. Christadoss, and N. Sarvetnick The Th2 Cytokine IL-4 Is Not Required for the Progression of Antibody-Dependent Autoimmune Myasthenia Gravis J. Immunol., September 15, 1998; 161(6): 2856 - 2862. [Abstract] [Full Text] [PDF] |
||||
![]() |
B. Balasa, C. Deng, J. Lee, L. M. Bradley, D. K. Dalton, P. Christadoss, and N. Sarvetnick Interferon gamma (IFN-gamma ) Is Necessary for the Genesis of Acetylcholine Receptor-induced Clinical Experimental Autoimmune Myasthenia gravis in Mice J. Exp. Med., August 4, 1997; 186(3): 385 - 391. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. M. Gomez, R. Maselli, J. E. Gundeck, M. Chao, J. W. Day, S. Tamamizu, J. A. Lasalde, M. McNamee, and R. L. Wollmann Slow-Channel Transgenic Mice: A Model of Postsynaptic Organellar Degeneration at the Neuromuscular Junction J. Neurosci., June 1, 1997; 17(11): 4170 - 4179. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |