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

Tuzun E., SAINI S. S., MORGAN B. P., CHRISTADOSS P.

JOURNAL OF NEUROIMMUNOLOGY, cilt.181, ss.29-33, 2006 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 181
  • Basım Tarihi: 2006
  • Doi Numarası: 10.1016/j.jneuroim.2006.07.016
  • Dergi Adı: JOURNAL OF NEUROIMMUNOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.29-33
  • Anahtar Kelimeler: myasthenia gravis, experimental autoimmune myasthenia gravis, CD59, complement, autoimmunity, DISEASE SEVERITY, GENETIC-EVIDENCE, CELL ACTIVATION, MICE, INVOLVEMENT, INDUCTION, DELETION
  • İstanbul Üniversitesi Adresli: Hayır

Özet

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 1gG1, 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. (c) 2006 Elsevier B.V. All rights reserved.