Abstract
Myasthenia gravis (MG) and its experimental animal model, experimental autoimmune myasthenia gravis (EAMG), are immune disorders characterized by circulating antibodies and lymphocyte autoreactivity to nicotinic acetylcholine receptor (AChR). Although the production of acetylcholine receptor specific antibodies is directly attributed to B cells, there is extensive evidence that T cells have a key role in the etiopathology of the disease in humans and animals [1-4]. Since the α-subunit of the AChR was shown to be predominant for T cell epitopes [2], we have used peptides representing different sequences of the human AChR α-subunit to study the role of T cells in the initiation, development and immunomodulation of myasthenia gravis.
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Pass-Rozner, M., Faber-Elmann, A., Sela, M., Mozes, E. (2000). Immunomodulation of Myasthenia Gravis Associated Autoimmune Responses by an Altered Peptide Ligand: Mechanisms of action. In: Christadoss, P. (eds) Myasthenia Gravis. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4060-7_17
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DOI: https://doi.org/10.1007/978-94-011-4060-7_17
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