Genetic evidence for the involvement of Fcγ receptor III in experimental autoimmune myasthenia gravis pathogenesis

Erdem Tüzün, Shamsher S. Saini, Huan Yang, Dhivyaa Alagappan, Stephen Higgs, Premkumar Christadoss

Research output: Contribution to journalArticlepeer-review

17 Scopus citations

Abstract

Immune complexes and classical complement pathway play vital roles in experimental autoimmune myasthenia gravis (EAMG). To analyze the role of immune complex receptors in EAMG, FcγRIII knockout (KO) mice were immunized with AChR and were found out to be resistant to EAMG induction. This was associated with reduced neuromuscular junction deposits, lymph node cell (LNC) IL-6 production and serum complement levels. EAMG resistance of anti-C1q Ab-administered mice was also associated with reduced LNC IL-6 production and neuromuscular junction deposits, indicating C1q involvement in EAMG resistance. The data provide the first direct genetic evidence for Fcγ receptor involvement in EAMG pathogenesis.

Original languageEnglish (US)
Pages (from-to)157-167
Number of pages11
JournalJournal of Neuroimmunology
Volume174
Issue number1-2
DOIs
StatePublished - May 1 2006

Keywords

  • Autoimmunity
  • C1q
  • Experimental autoimmune myasthenia gravis
  • Fc receptors
  • Myasthenia gravis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Fingerprint Dive into the research topics of 'Genetic evidence for the involvement of Fcγ receptor III in experimental autoimmune myasthenia gravis pathogenesis'. Together they form a unique fingerprint.

Cite this