Tumor necrosis factor receptor p55 and p75 deficiency protects mice from developing experimental autoimmune myasthenia gravis

Elzbieta Goluszko, Caishu Deng, Mathilde A. Poussin, Premkumar Christadoss

Research output: Contribution to journalArticle

34 Scopus citations

Abstract

The precise pathogenic role of proinflammatory cytokines belonging to the tumor necrosis factor (TNF) family has not been investigated yet in antibody-mediated myasthenia gravis (MG) and experimental autoimmune myasthenia gravis (EAMG). In this study we report that TNF receptor p55-/- p75-/- mice were resistant to the development of clinical EAMG induced by acetylcholine receptor (AChR) immunizations. The resistance was associated with reduced serum levels of IgG, IgG1, IgG2a, and IgG2b anti-AChR antibody isotypes. However, IgM anti-AChR antibodies were not reduced, suggesting defective anti-AChR IgG class switching in TNF receptor p55-/- p75-/- mice. We thus demonstrate the genetic evidence for the role of TNF receptor p55 and p75 in EAMG pathogenesis, and their requirement for the generation of anti-AChR IgG antibodies.

Original languageEnglish (US)
Pages (from-to)85-93
Number of pages9
JournalJournal of Neuroimmunology
Volume122
Issue number1-2
DOIs
StatePublished - Jan 29 2002

Keywords

  • Autoimmunity
  • Lymphotoxin-α
  • Myasthenia gravis
  • TNF receptors
  • TNF-α

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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