Abstract
Myasthenia gravis (MG) is an autoimmune disorder of the neuromuscular junction in which antibodies to the acetylcholine receptor (anti-AChR Ab) lead to muscle weakness and fatigability [1]. MG is treated with corticosteroids and immunosuppressive drugs which exert a non-specific action on the immune system. Moreover, their efficacy is frequently limited, and sometimes overwhelmed, by drug toxicity [2]. Experimental autoimmune MG (EAMG), the animal model of human myasthenia, is a T cell-dependent, B cell-mediated disorder suitable for the investigation of new therapeutic strategies. Indeed, data available on the structure and immunological recognition of the nicotinic AChR allow the design of antigen-specific approaches potentially able to modulate the autoimmune response to the AChR.
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© 2000 Springer Science+Business Media Dordrecht
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Baggi, F. et al. (2000). Oral Administration of Peptide Tαl46-162 Prevents EAMG in Mice. In: Christadoss, P. (eds) Myasthenia Gravis. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4060-7_14
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DOI: https://doi.org/10.1007/978-94-011-4060-7_14
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