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T cells from patients with Hodgkin's disease have a defective T-cell
receptor zeta chain expression that is reversible by T-cell stimulation
with CD3 and CD28
C Renner, S Ohnesorge, G Held, S Bauer, W Jung, JP Pfitzenmeier and M Pfreundschuh
Medical Department I, University of the Saarland, Homburg, Germany.
To investigate the mechanisms underlying the deficiency of T lymphocytes
from patients with Hodgkin's disease, we investigated the expression of the
T-cell receptor (TCR) zeta chain in patients with Hodgkin's disease. By
flow cytometry using an anti-zeta chain monoclonal antibody, peripheral
blood T lymphocytes from patients with untreated Hodgkin's disease were
shown to express decreased levels of the TCR zeta chain. After stimulation
by combined CD3 and CD28 cross- linking, T cells from Hodgkin's disease
patients upregulated zeta chain protein expression to normal values within
48 hours and achieved a cytolytic potential and levels of interleukin
(IL)-2 secretion that were not different from T cells obtained from healthy
controls. These results show that downregulation of the TCR zeta chain in
Hodgkin's T lymphocytes is a reversible event. Costimulation of CD3 and
CD28 is a novel approach for overcoming the T-cell deficiency in Hodgkin's
disease and might be exploited clinically. As upregulation of the zeta
chain can also be achieved using bispecific monoclonal antibodies (BI-
MoAbs) with specificity for tumor antigens and CD3 and CD28, respectively,
an immunotherapy with CD3/CD30 and CD28/CD30 Bi-MoAbs may overcome and
should therefore, not be jeopardized by the inherent T- cell deficiency in
patients with Hodgkin's disease.
Volume 88,
Issue 1,
pp. 236-241,
07/01/1996
Copyright © 1996 by The American Society of Hematology
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