Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis

Elzbieta Goluszko, Peter Hjelmström, Caishu Deng, Mathilde A. Poussin, Nancy H. Ruddle, Premkumar Christadoss

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

A complete prevention of clinical experimental autoimmune myasthenia gravis (EAMG) was observed in lymphotoxin (LT)-α deficient (LT-α-/-) mice compared to LT-α+/+ mice when immunized with acetylcholine receptor. However, only a partial prevention of clinical EAMG incidence was observed in LT-β-/- mice compared to LT-β+/+ mice. LT-α-/- and LT-β-/- mice had lower mean titers of total IgG, IgG1, IgG2a and IgG2b and higher or equal mean titers of IgM anti-AChR antibodies compared to controls. Therefore, LT-α-/- and LT-β-/- AChR immunized mice are capable of mounting a primary (IgM) humoral immune response to AChR, but are less capable of switching to the pathogenic anti-AChR IgG isotypes. LT could play a significant role in the pathogenesis of myasthenia gravis.

Original languageEnglish (US)
Pages (from-to)109-118
Number of pages10
JournalJournal of Neuroimmunology
Volume113
Issue number1
DOIs
StatePublished - Feb 1 2001

Keywords

  • Acetylcholine receptors
  • Autoimmunity
  • Cytokines
  • Lymphotoxins
  • Myasthenia gravis
  • TNF receptors

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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