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

Jing Li, Huibin Qi, Erdem Tüzün, Windy Allman, Vuslat Yilmaz, Shamsher S. Saini, Feza Deymeer, Güher Saruhan-Direskeneli, Premkumar Christadoss

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)40-45
Number of pages6
JournalJournal of Neuroimmunology
Issue number1-2
StatePublished - Mar 31 2009
Externally publishedYes


  • Autoimmunity
  • Complement
  • Lectin pathway
  • Mannose binding lectin
  • Myasthenia gravis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology


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