C5a is not involved in experimental autoimmune myasthenia gravis pathogenesis

Huibin Qi, Erdem Tüzün, Windy Allman, Shamsher S. Saini, Zurina R. Penabad, Silvia Pierangeli, Premkumar Christadoss

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


C5 deficient mice are highly resistant to experimental autoimmune myasthenia gravis (EAMG) despite intact immune response to acethylcholine receptor (AChR), validating the pivotal role played by membrane attack complex (MAC, C5b-9) in neuromuscular junction destruction. To distinguish the significance of C5a from that of C5b in EAMG pathogenesis, C5a receptor (C5aR) knockout (KO) and wild-type (WT) mice were immunized with AChR to induce pathogenic anti-AChR antibodies. In contrast with C5 deficient mice, C5aR KO mice were equally susceptible to EAMG as WT mice and exhibited comparable antibody and lymphocyte proliferation response to AChR implicating that C5a is not involved in EAMG development.

Original languageEnglish (US)
Pages (from-to)101-106
Number of pages6
JournalJournal of Neuroimmunology
Issue number1-2
StatePublished - May 30 2008


  • Autoimmunity
  • C5a
  • C5a receptor
  • Myasthenia gravis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology


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