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W Digel, W Schoniger, M Stefanic, H Janssen, C Buck, M Schmid, A Raghavachar and F Porzsolt
Department of Internal Medicine III, University of Ulm, FRG.
Recombinant tumor necrosis factor-alpha (TNF-alpha) is a cytokine that
induces proliferation of neoplastic B cells from patients with chronic
lymphocytic leukemia (CLL). To gain insight into the mechanisms involved in
regulating TNF responsiveness, we have examined TNF receptor expression on
neoplastic B-CLL cells. We have demonstrated that freshly isolated
neoplastic B cells from patients with CLL did not express TNF receptors.
After 1 day of incubation in culture medium, TNF receptors were detectable
in the range of 540 to 1,500/cell. Kinetic experiments revealed that
receptor expression was half-maximal after 3 hours of culturing and
required de novo protein synthesis. The Scatchard plots of TNF-alpha
binding indicated a single set of high- affinity TNF receptors with a
dissociation constant of 70 pmol/L. TNF receptor expression in vitro was
found in all examined cases. All cytokines tested, with the exception of
IL-2, did not influence the expression of TNF receptors. The TNF receptor
expression is enhanced in B-CLL cells cultured in the presence of
interleukin-2 when compared with the receptor expression of cells cultured
in medium alone. Our data suggest that neoplastic B-CLL cells in patients
with stable disease do not express TNF receptors in vivo and that an
unknown mechanism suppressing TNF receptor expression in vivo may play a
role in growth regulation of neoplastic B cells.
This article has been cited by other articles:
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| Copyright © 1990 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
