Inhibitory IgG receptor FcγRIIB fails to inhibit experimental autoimmune myasthenia gravis pathogenesis

Jing Li, Erdem Tüzün, Xiong Rong Wu, Hui Bin Qi, Windy Allman, Shamsher S. Saini, Premkumar Christadoss

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Deficiency of the inhibitory FcγRIIB renders mice susceptible to autoimmune disorders characterized with cellular infiltration of target tissue. To analyze the role of FcγRIIB in an antibody-mediated autoimmune disease, experimental autoimmune myasthenia gravis (EAMG), FcγRIIB knockout (KO) and wild-type mice were immunized with acetylcholine receptor (AChR). In contrast with previous reports, FcγRIIB KO mice were mildly resistant to EAMG despite preserved anti-AChR antibody production and neuromuscular junction complement deposition capacity. EAMG resistance was associated with reduced lymph node cell IL-6 and IL-10 production and increased CD4+CD25+ cell ratios in lymph nodes. Our data suggest that FcγRIIB promotes antibody-mediated autoimmunity.

Original languageEnglish (US)
Pages (from-to)44-53
Number of pages10
JournalJournal of Neuroimmunology
Volume194
Issue number1-2
DOIs
StatePublished - Feb 1 2008

Keywords

  • Autoimmunity
  • FcγRIIB
  • IL-10
  • IL-6
  • Myasthenia gravis

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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