Myasthenia gravis (MG) is an autoimmune disease mediated by antibodies to nicotinic acetylcholine receptor (AChR) interfering with the neuromuscular transmission. Experimental autoimmune MG serves as an excellent animal model to study possible therapeutic modalities for MG. This review will focus on the different ways to turn off the autoimmune response to AChR, which results in suppression of myasthenia. This paper will describe the use of fragments or peptides derived from the AChR, antigen-presenting cells and anti-T cell receptor antibodies, and will discuss the underlying mechanisms of action. Finally, the authors propose new promising therapeutic prospects, including treatment based on the modulation of regulatory T cells, which have recently been found to be functionally defective in MG patients.
Bibliographical noteFunding Information:
These studies were supported by grants from the National Institutes of Health (NS39869), the European Commission (QLG1-CT-2001-10918 and QLRT-2001-00225), the Muscular Dystrophy Association (MDA 3826) and by the Association Française Contre les Myopathies. SBA was the recipient of a Weston Professorship from the Weizmann Institute.
- Acetylcholine receptor
- Dendritic cells
- Myasthenia gravis
- Regulatory cells
- T cells