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Inhibitory effect of interleukin-4 on the in vitro growth of Ph1- positive
acute lymphoblastic leukemia cells
M Okabe, Y Kuni-eda, T Sugiwura, M Tanaka, T Miyagishima, I Saiki, T Minagawa, M Kurosawa, T Itaya and T Miyazaki
Third Department of Internal Medicine, School of Medicine, Hokkaido
University, Sapporo, Japan.
We investigated the effect of recombinant human interleukin-4 (rhIL-4) on
the in vitro growth of human leukemia cells in liquid culture and 3H-
thymidine incorporation and found inhibitory effects on the growth of
leukemic cells from patients with Ph1-positive acute lymphoblastic leukemia
(Ph1 ALL) and three Ph1 ALL cell lines. However, no inhibitory effects were
seen in Ph1-positive leukemic cell lines derived from patients with chronic
myelogenous leukemia in blast crisis and various types of Ph1-negative
leukemia cells, including B-lineage leukemia cells. In a flow cytometry
assay of IL-4 receptor (IL-4R), all three Ph1-positive ALL cell lines
showed the presence of IL-4R on their cell surfaces, and the IL-4-dependent
inhibition on the growth of Ph1- positive ALL cells was abrogated by the
addition of either monoclonal or polyclonal antibodies against rhIL-4.
Other cytokines, including IL- 2, IL-3, granulocyte-macrophage
colony-stimulating factor (CSF), granulocyte-CSF, and IL-6, showed no
inhibitory effects on the growth of Ph1-ALL cells, but tumor necrosis
factor-alpha (TNF-alpha) and interferon (IFN)-alpha, -beta, and -gamma
displayed slight inhibitory effects in a high concentration. The growth
inhibition induced by rhIL- 4 in the Ph1-positive ALL cells was not
abrogated by the addition of antibodies against either IFN-gamma or
TNF-alpha. Furthermore, these cells showed no significant production of
IFN-alpha, -beta, or -gamma or TNF-alpha after exposure to rhIL-4, thus
indicating that the growth inhibition of Ph1-positive ALL cells by rhIL-4
is not associated with IL-4-stimulating production of these factors. rhIL-4
caused significant inhibition of the tyrosine kinase activity in these
Ph1-positive ALL cells, similar to Herbimycin A, an inhibitor of tyrosine
kinase that inhibited the tyrosine kinase activity in these cells. Our
finding suggests that the clinical evaluation of rhIL-4 may offer promising
therapeutic possibilities for patients with Ph1-positive ALL.
Volume 78,
Issue 6,
pp. 1574-1580,
09/15/1991
Copyright © 1991 by The American Society of Hematology
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