International Immunology, Vol 10, 911-921, Copyright © 1998 by Oxford University Press
T Takeuchi, K Tsuzaka, M Pang, K Amano, J Koide and T Abe
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
zeta 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 zeta chain expression, we
found two patients with pronounced TCR zeta 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
468503, 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 zeta chain, the transcript lacking exon 7 may be responsible
for altered signal transduction via TCR in these SLE patients.
ARTICLES
TCR zeta chain lacking exon 7 in two patients with systemic lupus erythematosus
Department of Internal Medicine, Saitama Medical Center, Saitama Medical School, Kawagoe, Japan.
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