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Interleukin-6 inhibits the proliferation of B-chronic lymphocytic leukemia
cells that is induced by tumor necrosis factor-alpha or -beta
D Aderka, Y Maor, D Novick, H Engelmann, Y Kahn, Y Levo, D Wallach and M Revel
Department of Molecular Genetics and Virology, Weizmann Institute of
Science, Rehovot, Israel.
Tumor necrosis factor (TNF-alpha) acts as a growth stimulatory factor on
leukemic B lymphocytes from many patients with chronic lymphocytic leukemia
(CLL). Because TNF induces production of interleukin-6 (IL-6), which has
been shown to be a growth factor for myeloma and other transformed B cells,
we examined the possibility that IL-6 mediates the growth-stimulatory
effect of TNF on B-CLL cells. In fact, we found that IL-6 is an inhibitor
of B-CLL growth. The addition of recombinant human IL-6 markedly decreased
the TNF-induced B-CLL growth, and this decrease was even greater when
soluble IL-6 receptor, known to act as IL-6 agonist, was added with
recombinant IL-6. Conversely, neutralizing monoclonal antibodies to IL-6
and to the IL-6 receptor potentiated the growth stimulation of TNF on B-CLL
cells, in line with the possibility that IL-6 functions as a negative
feedback regulator of an autocrine TNF action on these B-leukemic cells.
Evidence is presented that production of IL-6 by monocytes and B cells of
CLL patients is low, suggesting that administration of IL-6 may be
beneficial in CLL to reduce the eventual growth stimulation by TNF and,
possibly, also the deficiency in platelets and Ig production in this
disease.
Volume 81,
Issue 8,
pp. 2076-2084,
04/15/1993
Copyright © 1993 by The American Society of Hematology
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