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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 Here we summarize published and unpublished experience using the AChR passive transfer MG model in mice, rats and rhesus monkeys, and give recommendations for the design of preclinical studies in order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.

Original publication

DOI

10.1016/j.expneurol.2015.02.025

Type

Journal article

Journal

Exp Neurol

Publication Date

08/2015

Volume

270

Pages

3 - 10

Keywords

Acetylcholine receptor antibody, Autoimmune disease, Myasthenia gravis, Neuromuscular junction, Passive transfer model, Animals, Autoantibodies, Autoantigens, Guidelines as Topic, Humans, Macaca mulatta, Mice, Myasthenia Gravis, Autoimmune, Experimental, Rats, Receptors, Cholinergic