Preferential production of IgG1, IL-4 and IL-10 in MuSK-immunized mice
- 1 April 2014
- journal article
- research article
- Published by Elsevier in Clinical Immunology
- Vol. 151 (2) , 155-163
Abstract
No abstract availableKeywords
Funding Information
- Myasthenia Gravis Foundation of America
- Association Française contre les Myopathies
- Muscular Dystrophy Association (109S353)
- Scientific and Technological Research Council of Turkey (TUBITAK)
- NSRF “Thalis” Autoimmunity Grant of Greece
This publication has 23 references indexed in Scilit:
- Animal models of antimuscle‐specific kinase myastheniaAnnals of the New York Academy of Sciences, 2012
- Muscle-specific kinase myasthenia gravis IgG4 autoantibodies cause severe neuromuscular junction dysfunction in miceBrain, 2012
- Divalent and monovalent autoantibodies cause dysfunction of MuSK by distinct mechanisms in a rabbit model of myasthenia gravisJournal of Neuroimmunology, 2012
- Antibodies against Muscle-Specific Kinase Impair Both Presynaptic and Postsynaptic Functions in a Murine Model of Myasthenia GravisThe American Journal of Pathology, 2012
- Complement and cytokine based therapeutic strategies in myasthenia gravisJournal of Autoimmunity, 2011
- IgG1 antibodies to acetylcholine receptors in ‘seronegative’ myasthenia gravis†Brain, 2008
- Regulation of Anaphylactic IgG1 Antibody Production by IL-4 and IL-10International Archives of Allergy and Immunology, 2006
- Adjuvant-dependent modulation of Th1 and Th2 responses to immunization with beta-amyloidInternational Immunology, 2003
- Animal Models of Myasthenia GravisClinical Immunology, 2000
- Myasthenic Antibodies Cross-Link Acetylcholine Receptors to Accelerate DegradationNew England Journal of Medicine, 1978