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| Research article summary (published 12 Aug 1998): |
Role of the target organ in determining susceptibility to experimental autoimmune myasthenia gravis.
Full Abstract
Injection of anti-AChR antibodies in passive transfer experimental autoimmune myasthenia gravis (EAMG) results in increased degradation of acetylcholine receptor (AChR) and increased synthesis of AChR alpha-subunit mRNA. Passive transfer of anti-Main Immunogenic Region (MIR) mAb 35 in aged rats does not induce clinical signs of disease nor AChR loss. The expression of the AChR subunit genes was analyzed in susceptible and resistant rats. In aged EAMG resistant rats, no increase in the amount of AChR alpha-subunit mRNA was measured. In vivo AChR degradation experiments did not show any increase in AChR degradation rates in aged resistant rats, in contrast to young susceptible rats. Taken together, these data demonstrate that resistance of the AChR protein to antibody-mediated degradation is the primary mechanism that accounts for the resistance to passive transfer EAMG in aged rats.
Author information
Author/s: Hoedemaekers, A (A); Bessereau, J L (JL); Graus, Y (Y); Guyon, T (T); Changeux, J P (JP); Berrih-Aknin, S (S); van Breda Vriesman, P (P); De Baets, M H (MH);
Affiliation: Maastricht University, Department of Immunology, The Netherlands.
Journal and publication information
Publication Type: Journal Article; Research Support, Non-U.S. Gov't
Journal: Journal of neuroimmunology (J Neuroimmunol), published in NETHERLANDS. (Language: eng)
Reference: 1998-Aug; vol 89 (issue 1-2) : pp 131-41
Dates: Created 1998/09/10; Completed 1998/09/10; Revised 2006/11/15;
PMID: 9726835, status: MEDLINE (last retrieval date: 2/18/2009, IMS Date: )
Sourced from the National Library of Medicine. Abstract text and other information may be subject to copyright.
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