Document Type
Journal Article
Publication Date
3-2-2015
Journal
Experimental Neurology
Volume
270
Inclusive Pages
3-10
DOI
10.1016/j.expneurol.2015.02.025
Abstract
Antibodies against the muscle acetylcholine receptor (AChR) are the most common cause of myasthenia gravis (MG). Passive transfer of AChR antibodies from MG patients into animals reproduces key features of human disease, including antigenic modulation of the AChR, complement-mediated damage of the neuromuscular junction, and muscle weakness. Similarly, AChR antibodies generated by active immunization in experimental autoimmune MG models can subsequently be passively transferred to other animals and induce weakness. The passive transfer model is useful to test therapeutic strategies aimed at the effector mechanism of the autoantibodies. Here we summarize published and unpublished experience using the AChR passive transfer MG model in mice, rats and rhesus monkeys, and give recommendations for the design of preclinical studies in order to facilitate translation of positive and negative results to improve MG therapies.
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
APA Citation
Epub ahead of print
Peer Reviewed
1
Open Access
1
Included in
Medical Pharmacology Commons, Medical Physiology Commons, Nervous System Diseases Commons
Comments
Reproduced with permission of Elsevier B.V. Experimental Neurology