Complement regulator CD59 deficiency fails to augment susceptibility to actively induced experimental autoimmune myasthenia gravis

Erdem Tüzün, Shamsher S. Saini, B. Paul Morgan, Premkumar Christadoss

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

Complement deficient mice are resistant to experimental autoimmune myasthenia gravis (EAMG), suggesting a pivotal role for the membrane attack complex (MAC) in EAMG pathogenesis. To test the significance of MAC regulation in EAMG pathogenesis, CD59 KO and wild type mice were immunized with acetylcholine receptor (AChR). Interestingly, deletion of CD59, the regulator of MAC assembly, failed to augment EAMG susceptibility. The CD59 KO mice had reduced serum anti-AChR IgG1, IgG2b and complement levels. Their lymph node cell IL-2 production and lymphocyte proliferation response to AChR were reduced. The data challenge the current paradigm that CD59 is solely involved in MAC regulation and suggest a role for this molecule in antigen-driven T cell and B cell activation.

Original languageEnglish (US)
Pages (from-to)29-33
Number of pages5
JournalJournal of Neuroimmunology
Volume181
Issue number1-2
DOIs
StatePublished - Dec 1 2006

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Keywords

  • Autoimmunity
  • CD59
  • Complement
  • Experimental autoimmune myasthenia gravis
  • Myasthenia gravis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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