Titre :
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Prevention of experimental autoimmune myasthenia gravis by anti-C1Q antibody is associated with reduced anti-AChR IgG2b, IL-6 and IFN-alpha production (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) ;
Tüzün E ;
Saini S ;
Yang H ;
Higgs S ;
Christadoss P
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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. 252
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Langues:
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Anglais
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Mots-clés :
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anticorps
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anticorps anti-récepteur nicotinique
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colloque
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complément C3
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complément C4
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complexe d'attaque membranaire
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IL-6
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interféron alpha
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jonction neuromusculaire
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modèle animal
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myasthénie auto-immune
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prise en charge thérapeutique
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souris
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Résumé :
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Communication n° 5 Introduction: The classical complement pathway (CP) is involved in the induction of experimental autoimmune myasthenia gravis (EAMG) induced by acetylcholine receptor (AChR) immunization. Objective: To delineate the significance of CP manipulation for myasthenia gravis prevention and treatment. Methods: C57BL/6 mice were treated with anti-C1q monoclonal antibodies (anti-C1q Ab) before and after AChR immunization. Results: Anti-C1q Ab-administered mice had reduced EAMG incidence and severity as compared to control isotype antibody-administered mice. This resistance in anti-C1q Ab-administered mice was associated with reduced serum anti-AChR IgG2b levels, lymph node cell IL-6 and IFN-? production. Despite reduced deposits of IgG, C3 and membrane attack complex in the neuromuscular junction, anti-C1q Ab-administered mice had elevated circulating immune complex, C1q and C3 levels and comparable C4 levels in the serum. Anti-C1q Ab administration did not suppress PNA+ spleen cell counts and AChR-specific lymphocyte proliferation capacities and thus did not induce immune deficiency as seen with other immunosuppressive treatment methods for autoimmune diseases. Conclusion: Our results demonstrate for the first time that an autoimmune disease can be prevented by an antibody that is specifically directed against a CP component. Anti-C1q antibody prevented EAMG induction without abolishing humoral immunity and partially inhibiting proinflammatory cytokine production. Therefore, inhibition of classical complement pathway might constitute an effective therapy for MG. Reduced LNC IL-6 production might lead to decreased anti-AChR IgG2b isotype production and this might be associated with fewer NMJ deposits and reduced severity of EAMG.
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