Mannose-binding lectin pathway is not involved in myasthenia gravis pathogenesis

LI J., QI H., Tuzun E., ALLMAN W., Yilmaz V., SAINI S. S., ...More

Journal of Neuroimmunology, vol.208, pp.40-45, 2009 (SCI-Expanded) identifier identifier identifier

  • Publication Type: Article / Article
  • Volume: 208
  • Publication Date: 2009
  • Doi Number: 10.1016/j.jneuroim.2008.12.013
  • Journal Name: Journal of Neuroimmunology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.40-45
  • Keywords: Myasthenia gravis, Mannose binding lectin, Lectin pathway, Complement, Autoimmunity, COMPLEMENT ACTIVATION, ANTI-C1Q ANTIBODY, DEFICIENT MICE, MURINE MODEL, IN-VIVO, DISEASE, INDUCTION, PHENOTYPE, INJURY, CELL
  • Istanbul University Affiliated: Yes


Classical complement pathway factor, C4 is required for experimental autoimmune myasthenia gravis (EAMG) pathogenesis. C4 is also a central component of the mannose binding lectin (MBL) pathway suggesting that this pathway might also be involved in MG pathogenesis. However, MBL gene deficient mice displayed intact anti-acetylcholine receptor (AChR)-immune response and neuromuscular junction (NMJ) IgG and complement accumulation following AChR-immunization. Moreover, no significant difference was observed between the serum MBL levels of 77 anti-AChR antibody positive generalized MG patients and 105 healthy controls. Therefore, MBL pathway does not play a role in EAMG/MG pathogenesis. © 2009 Elsevier B.V. All rights reserved.