Titre :
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New aspects on the pathophysiology of human myasthenia gravis (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) ;
Lefvert AK ;
Kakoulidou M ;
Sakthivel P ;
Wang XB ;
Zhao X ;
Pirskanen R
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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. 258
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Langues:
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Anglais
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Mots-clés :
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autoanticorps
;
colloque
;
cytokine
;
gène TNF
;
IL-1
;
lymphocyte T
;
mutation génétique
;
myasthénie auto-immune
;
récepteur nicotinique
;
souris
;
thymome
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Résumé :
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Communication n° 446 Introduction : Recent research shows that the autoantibodies are not the only determining factors for the disease. Thus, we have focused on other pathogenic mechanisms. Results : Identical twins discordant for myasthenia have the same autoantibody repertoires, but only the myasthenic twins show T cell reactivity against the acetylcholine receptor. Myasthenia is associated to high-secretory variants of the IL-1 and TNF genes. The mouse lacking IL1 is resistant to development of experimental myasthenia and TNF blockade can be used to treat patients. Variants of the T cell cofactor CTLA-4 gene leading to decreased expression/function of CTLA-4 are also associated to myasthenia, especially to patients with thymomas. Conclusions : Human myasthenia gravis is dependent not only on acetylcholine receptor autoantibodies but also on cytokines and T cell cofactors
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