Warning: The NCBI web site requires JavaScript to function. more...
Generate a file for use with external citation management software.
CNRS UMR 8078, Universite Paris Sud, IPSC Hôpital Marie Lannelongue, 133 Avenue de la Résistance, 92350 Le Plessis Robinson, France. sonia.berrih@ccml.u-psud.fr
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.
Images from this publication.See all images (3) Free text
Your browsing activity is empty.
Activity recording is turned off.
Turn recording back on