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Journal Article

Increased gene expression of acetylcholine receptor and myogenic factors in passively transferred experimental autoimmune myasthenia gravis

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Kues,  Winfried
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Witzemann,  Veit
Department of Molecular Neurobiology, Max Planck Institute for Medical Research, Max Planck Society;
Working Group Witzemann / Koenen, Max Planck Institute for Medical Research, Max Planck Society;
Molecular anatomy of the neuromuscular junction, Max Planck Institute for Medical Research, Max Planck Society;
Department of Cell Physiology, Max Planck Institute for Medical Research, Max Planck Society;

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Citation

Asher, O., Kues, W., Witzemann, V., Tzartos, S. J., Fuchs, S., & Souroujon, M. C. (1993). Increased gene expression of acetylcholine receptor and myogenic factors in passively transferred experimental autoimmune myasthenia gravis. The Journal of Immunology, 151(11), 6442-6450. Retrieved from http://www.jimmunol.org/content/151/11/6442.


Cite as: http://hdl.handle.net/11858/00-001M-0000-0019-AAD0-C
Abstract
The passive transfer of myasthenia gravis by injection of mAb against muscle acetylcholine receptor (AChR) alpha−subunit, results in increased expression of AChR subunit genes, mainly at synaptic regions. The gene expression of AChR and of other muscle−specific proteins is regulated in a similar manner in passively transferred experimental autoimmune myasthenia gravis (EAMG) and in AChR−induced EAMG. Administration of AChR−specific mAb leads to a significant reduction in muscle AChR content and to an elevation in the mRNA levels corresponding to the adult, synaptic type of the receptor, as shown by Northern blot and in situ hybridization analyses. The mRNA levels of the myogenic factors myogenin and MRF4 are also increased moderately, whereas MyoD transcript levels remain unchanged. Thus, passive transfer of EAMG by mAb directed to defined epitopes of AChR alpha−subunit provides a suitable model for analyzing and following the cascade of molecular events triggered by anti−AChR immunopathologic antibodies and may shed light on the regulatory mechanisms underlying the human disease as well