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Mechanisms of tumor necrosis factor-granulocyte-macrophage colony-
stimulating factor-induced dendritic cell development
F Santiago-Schwarz, N Divaris, C Kay and SE Carsons
Winthrop-University Hospital, Mineola, NY.
In a previous report, we described that tumor necrosis factor (TNF) and
granulocyte-macrophage colony-stimulating factor (GM-CSF) synergistically
enhanced the development of dendritic cell (DC) progeny from early stem
cells and that there is a common monocyte-DC progenitor cell. Low levels of
DC were obtained with GM-CSF alone, and TNF by itself failed to induce stem
cell development. Here, we investigate mechanisms by which TNF and GM-CSF
institute increases in DC, and how these same molecules support later
stages of DC differentiation. We show that TNF is required as the first
signal, that there is upregulation of GM-CSF receptors (GM-CSFRs), and that
TNF inhibits the differentiation of colony-forming units-granulocyte. High
levels of GM- CSFR were always associated with conditions yielding a large
number of DC, and a kinetic analysis showed a close ontogenic relationship
between DC and GM-CSFR levels. The addition of anti-GM-CSF or anti-TNF
antibodies blocked synergistic responses related to DC development,
including high levels of GM-CSFRs. Anti-GM-CSF was the most potent
inhibitor of proliferation (80%) and macrophage, DC, and polymorphonuclear
(PMN) cell development. With polyclonal anti-TNF, inhibition was less
(35%), and there was a shift from myelomonocytic and DC to PMN progeny. Our
results support the concept that receptor upregulation is an important
mechanism for growth factor synergy. Our data also indicate that the
opposing effects of TNF on hematopoiesis contribute to the selection of the
DC pathway and emphasize the importance of GM-CSFRs not only in initiated
DC development, but also in controlling DC viability and function.
Volume 82,
Issue 10,
pp. 3019-3028,
11/15/1993
Copyright © 1993 by The American Society of Hematology
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