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Human granulocyte-monocyte colony-stimulating factor and interleukin 3
stimulate monocyte cytotoxicity through a tumor necrosis factor- dependent
mechanism
SA Cannistra, E Vellenga, P Groshek, A Rambaldi and JD Griffin
Division of Tumor Immunology, Dana-Farber Cancer Institute, Harvard Medical
School, Boston, MA 02115.
Human colony-stimulating factors (CSF) exert multiple effects on the
proliferation, differentiation, and function of myeloid lineage cells. In
this study, the effects of three recombinant human CSFs (granulocyte-
monocyte CSF [GM-CSF], interleukin 3 [IL-3], and granulocyte CSF [G- CSF])
on antibody-independent monocyte tumoricidal activity were investigated by
using WEHI 164 fibrosarcoma cells as monocyte-sensitive targets. None of
the CSFs directly induced monocyte cytotoxicity, although both GM-CSF and
IL-3 were found to significantly enhance monocyte killing in response to a
second stimulatory event (endotoxin). No effect was seen with G-CSF.
Antitumor necrosis factor antibody completely abolished CSF-enhanced
monocyte cytotoxicity, which suggests that this effect was mediated through
increased release of tumor necrosis factor (TNF). As previously shown for
GM-CSF, IL-3 was found to induce cytoplasmic accumulation of TNF messenger
RNA (mRNA) after 18 hours of exposure. These results suggest that GM-CSF
and IL-3 may stimulate monocyte killing indirectly by enhancing expression
of TNF mRNA, thereby leading to augmented TNF protein secretion in response
to a second activation signal.
Volume 71,
Issue 3,
pp. 672-676,
03/01/1988
Copyright © 1988 by The American Society of Hematology
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