TCR ζ chain lacking exon 7 in two patients with systemic lupus erythematosus

Tsutomu Takeuchi, Kensei Tsuzaka, Ming Pang, Kouichi Amano, Jun Koide, Tohru Abe

Research output: Contribution to journalArticle

65 Citations (Scopus)

Abstract

To address the molecular mechanism underlying the functional defects of peripheral T cells in systemic lupus erythematosus (SLE), we focused on early signaling events. We demonstrated that protein expression of the TCR ζ chain was significantly decreased in peripheral T cells from patients with SLE compared to normal controls and patients with systemic sclerosis (SSc). Among those patients showing decreased TCR ζ chain expression, we found two patients with pronounced TCR ζ chain abnormalities, including an aberrant 14 kDa form in one and only trace expression in the other. RT-PCR, SSCP and subsequent cloning of the transcripts revealed that bases 468-503, corresponding to exon 7, were deleted in both patients. Since exon 7 spans the GTP/GDP binding site and N-terminal tyrosine in the third ITAM domain of TCR ζ chain, the transcript lacking exon 7 may be responsible for altered signal transduction via TCR in these SLE patients.

Original languageEnglish
Pages (from-to)911-921
Number of pages11
JournalInternational immunology
Volume10
Issue number7
DOIs
Publication statusPublished - 1998 Jul 24
Externally publishedYes

Keywords

  • Autoimmunity
  • Human
  • Signal transduction
  • T lymphocytes
  • Tyrosine phosphorylation

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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