C5 gene influences the development of murine myasthenia gravis

P. Christadoss

Research output: Contribution to journalArticle

76 Scopus citations

Abstract

The influence of the C5 gene and C5 deficiency on murine experimental autoimmune myasthenia gravis (EAMG) susceptibility was evaluated. Two coisogenic strains, B10.D2/nSn (C5 sufficient) and B10.D2/oSn (C5 deficient), which are genetically identical except for the C5 gene locus, were immunized with acetylcholine receptors (AChR) in CFA to induce myasthenia gravis. Both strains had equivalent concentration of serum autoantibodies to muscle AChR and antibodies bound to muscle AChR. C5-sufficient B10.D2/nSn, but not C5-deficient B10.D2/oSn, demonstrated increased incidence of clinical disease and death and lost significant amounts of muscle AChR. Therefore, C5 deficiency in B10.D2/oSn prevented EAMG. C5 gene, which codes for C component C5, may influence EAMG pathogenesis through activation of the terminal lytic C sequence (C5 to C9) required for muscle AChR destruction, which is the primary pathology.

Original languageEnglish (US)
Pages (from-to)2589-2592
Number of pages4
JournalJournal of Immunology
Volume140
Issue number8
StatePublished - May 13 1988

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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