
Molecular abnormalities of T‐cells in systemic lupus erythematosus
Author(s) -
TAKEUCHI Tsutomu,
TSUZAKA Kensei,
KAMEDA Hideto,
AMANO Kouichi
Publication year - 2006
Publication title -
aplar journal of rheumatology
Language(s) - English
Resource type - Journals
eISSN - 1479-8077
pISSN - 0219-0494
DOI - 10.1111/j.1479-8077.2006.00239.x
Subject(s) - t cell receptor , medicine , immunology , pathogenesis , lupus erythematosus , t cell , exon , gene , biology , immune system , antibody , genetics
Substantial evidence supports that T‐cells play a central role in the pathogenesis of systemic lupus erythematosus (SLE). To explore the molecular basis of the defective function of SLE T‐cells, we focused on the signal transduction system via T‐cell antigen receptor (TCR) in peripheral blood T‐cells from SLE patients. Comprehensive analysis to identify the molecules responsible for the defects showed the expression of the TCR ζ chain was attenuated, or absent in more than half of SLE patients. Moreover, the aberrant transcripts of the TCR ζ chain, including spliced variants lacking exon 7 and with a short 3′‐UTR, were detected in SLE T‐cells. Although attenuated expression of the TCR ζ chain is also observed in patients with cancers, infections, and other autoimmune diseases, sustained attenuation of TCR ζ expression and aberrant transcripts are only observed in SLE. In this review we discuss the unique features of the TCR ζ defects in SLE.