Suppression of experimental autoimmune myasthenia gravis in IL-10 gene-disrupted mice is associated with reduced B cells and serum cytotoxicity on mouse cell line expressing AChR

Mathilde A. Poussin, Elzbieta Goluszko, Thomas K. Hughes, Sacha I. Duchicella, Premkumar Christadoss

Research output: Contribution to journalArticle

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To analyze the role of interleukin-10 (IL-10) in experimental autoimmune myasthenia gravis (EAMG) pathogenesis, we induced clinical EAMG in C57BL/6 and IL-10 gene-knockout (KO) mice. IL-10 KO mice had a lower incidence and severity of EAMG, with less muscle acetylcholine receptor (AChR) loss. AChR-immunized IL-10 KO mice showed a significantly higher AChR-specific proliferative response, altered cytokine response, lower number of class II-positive cells and B-cells, but a greater CD5+CD19+ population than C57BL/6 mice. The lower clinical incidence in IL-10 KO could be explained not by a reduction of the quantity, but by a possible difference in the pathogenicity of anti-AChR antibodies. Copyright (C) 2000.

Original languageEnglish (US)
Pages (from-to)152-160
Number of pages9
JournalJournal of Neuroimmunology
Issue number1-2
StatePublished - Nov 1 2000



  • Autoimmunity
  • IL-10
  • IL-10 gene knockout
  • Immunomodulation
  • Myasthenia gravis

ASJC Scopus subject areas

  • Immunology
  • Clinical Neurology
  • Immunology and Allergy
  • Neurology

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