Decreased expression of Src homology 2 domain-containing protein tyrosine phosphatase 1 reduces T cell activation threshold but not the severity of experimental autoimmune myasthenia gravis

Caishu Deng, Bo Wu, Huan Yang, Rehana Z. Hussain, Amy E. Lovett-Racke, Premkumar Christadoss, Michael K. Racke

Research output: Contribution to journalArticle

5 Scopus citations

Abstract

Myasthenia gravis (MG) and its murine model experimental autoimmune myasthenia gravis (EAMG) are T cell-dependent, antibody-mediated autoimmune diseases. Src homology 2 domain-containing protein tyrosine phosphatase 1 (SHP-1) is a cytosolic tyrosine phosphatase that is involved in regulating the T cell activation cascade from signals initiated through the TCR. To study the role of SHP-1 in EAMG pathogenesis, we immunized C57BL/6 (B6) mice heterozygous for deletion of the SHP-1 gene (mev+/-) and their littermate wild type B6 mice with torpedo acetylcholine receptor (TAChR). T cell proliferation and IFNγ production were significantly increased in B6.mev+/- mice after immunization with AChR compared to that of wild type littermates. However, clinical incidence and severity of the disease were not changed. There also were no significant differences in AChR-specific antibodies produced between wild type and mev+/- mice. These data suggest that deficiency in SHP-1 expression does decrease the activation threshold of autoreactive T cells in EAMG, but the increased frequency of autoreactive T cells does not aggravate EAMG in terms of clinical score, incidence, or antibody titers.

Original languageEnglish (US)
Pages (from-to)76-82
Number of pages7
JournalJournal of Neuroimmunology
Volume138
Issue number1-2
DOIs
StatePublished - May 2003

Keywords

  • Acetylcholine receptor
  • Auto-antibody
  • Experimental autoimmune myasthenia gravis
  • T cell activation
  • Tyrosine phosphatase

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

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