MuSK induced experimental autoimmune myasthenia gravis does not require IgG1 antibody to MuSK

Kucukerden M., Huda R., Tuzun E., Yilmaz A., Skriapa L., Trakas N., ...Daha Fazla

JOURNAL OF NEUROIMMUNOLOGY, cilt.295, ss.84-92, 2016 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 295
  • Basım Tarihi: 2016
  • Doi Numarası: 10.1016/j.jneuroim.2016.04.003
  • Dergi Adı: JOURNAL OF NEUROIMMUNOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.84-92
  • Anahtar Kelimeler: Myasthenia gravis, Experimental autoimmune myasthenia gravis, Muscle specific kinase, Anti-MuSK IgG, MuSK-binding B cell, MUSCLE-SPECIFIC KINASE, ACETYLCHOLINE-RECEPTORS, IMMUNIZED MICE, AUTOANTIBODIES, MECHANISMS, BINDING, MOUSE, MODEL, DYSFUNCTION, COMPLEMENT
  • İstanbul Üniversitesi Adresli: Evet

Özet

Sera of myasthenia gravis (MG) patients with muscle-specific receptor kinase-antibody (MuSK-Ab) predominantly display the non-complement fixing IgG4 isotype. Similarly, mouse IgG1, which is the analog of human IgG4, is the predominant isotype in mice with experimental autoimmune myasthenia gravis (EAMG) induced by MuSK immunization. The present study was performed to determine whether IgG1 anti-MuSK antibody is required for immunized mice to develop EAMG. Results demonstrated a significant correlation between clinical severity of EAMG and levels of MuSK-binding IgG1 +, IgG2 + and IgG3 + peripheral blood B cells in MuSK-immunized wild-type (WT) mice. Moreover, MuSK-immunized IgG1 knockout (KO) and WT mice showed similar EAMG severity, serum MuSK-Ab levels, muscle acetylcholine receptor concentrations, neuromuscular junction immunoglobulin and complement deposit ratios. IgG1 and IgG3 were the predominant anti-MuSK isotypes in WT and IgG1 KO mice, respectively. These observations demonstrate that non-IgG1 isotypes can mediate MuSK-EAMG pathogenesis. (C) 2016 Elsevier B.V. All rights reserved.