Titre :
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Clinical and immunological amelioration of chronic experimental autoimmune myasthenia gravis by antisense oligonucleotide treatment (abstract : congrès international de Myologie, 2005)
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contenu dans :
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Auteurs :
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Congrès international de myologie 2005 (International Congress of Myology 2005; 9-13 mai 2005; Nantes, France) ;
Brenner T ;
Hamra-Amitay Y ;
Sicsic C ;
Berrih-Aknin S
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Type de document :
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Article
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Année de publication :
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2005
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Pages :
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p. 253
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Langues:
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Anglais
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Mots-clés :
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acétylcholinestérase
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apoptose
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colloque
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jonction neuromusculaire
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modèle animal
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muscle squelettique
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myasthénie auto-immune
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oligonucléotide antisens
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prise en charge thérapeutique
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pyridostigmine
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rat
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récepteur nicotinique
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Résumé :
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Communication n° 106 Myasthenia gravis is an antibody-mediated, autoimmune neuromuscular disease in which the nicotinic acetylcholine receptor (AChR) is the major autoantigen. The typical neuromuscular junction symptoms can be transiently alleviated by acetylcholinesterase (AChE) inhibitors (such as pyridostigmine). Previously we found that long-term treatment of experimental autoimmune myasthenia gravis (EAMG) rats with antisense oligodeoxynucleotides suppressing AChE biosynthesis (EN101), improved muscle activity as well as clinical symptoms of the disease. In the present study we focused on the effect of EN101 treatment on the typical immunological processes occurring in EAMG. Repeated oral administration of EN101 for a month reduced the anti-rat AChR antibody level by 50%. In addition, incubation of T-cells with EN101 resulted in reduction in the proliferation rate and induction of apoptosis. EN101 also lowered total IgG antibody production by spleen cells. Our results show the beneficial effect of oral EN101 treatment on EAMG immunological parameters and highlight the potential advantage of gene-targeted drug therapy.
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