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Modulation of cell proliferation and cytokine production in acute
myeloblastic leukemia by interleukin-1 receptor antagonist and lack of its
expression by leukemic cells
A Rambaldi, M Torcia, S Bettoni, E Vannier, T Barbui, AR Shaw, CA Dinarello and F Cozzolino
Division of Hematology, Ospedali Riuniti, Bergamo, Italy.
Interleukin-1 (IL-1) is spontaneously produced by acute myeloblastic
leukemia (AML) cells. IL-1 also induces synthesis of colony-stimulating
factors (CSFs) and sustains leukemic growth. An IL-1-specific inhibitor has
been recently purified and cloned; this molecule binds to IL-1 receptors
but has no IL-1 activity, fulfilling the characteristics of an IL-1
receptor antagonist (IL-1ra). Because high-affinity binding sites for
IL-1ra were shown on AML cells by radioligand binding studies, we studied
the effect of IL-1ra on the proliferative activity of blast cells isolated
from 16 cases of AML. In each case, spontaneous proliferation was inhibited
by addition of the IL-1ra in a dose- dependent manner (1 to 100 ng/mL).
Culture supernatants of unstimulated leukemic cells contained IL-1 beta and
granulocyte-macrophage CSF (GM- CSF), but when incubated with the IL-1ra, a
reduction or disappearance of GM-CSF was observed in 8 of 10 cases, whereas
spontaneous IL-1 production was reduced in four of seven cases. By Northern
hybridization, IL-1 beta gene transcripts were shown in 20 of 23 AML cases,
whereas IL-1ra-specific messenger RNA was present in only two of the
patients studied. These data show a role for IL-1 in the spontaneous
proliferation and cytokine production of AML cells and suggest that an
imbalanced synthesis of IL-1 and of its natural receptor antagonist may
contribute to the unrestricted growth of AML cells.
Volume 78,
Issue 12,
pp. 3248-3253,
12/15/1991
Copyright © 1991 by The American Society of Hematology
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