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Bifunctional effects of tumor necrosis factor alpha (TNF alpha) on the
growth of mature and primitive human hematopoietic progenitor cells:
involvement of p55 and p75 TNF receptors
LS Rusten, FW Jacobsen, W Lesslauer, H Loetscher, EB Smeland and SE Jacobsen
Department of Immunology, Norwegian Radium Hospital, Oslo.
Tumor necrosis factor alpha (TNF alpha) has previously been reported to
have both inhibitory and stimulatory effects on hematopoietic progenitor
cells. Specifically, TNF alpha has been proposed to stimulate early
hematopoiesis in humans. In the present study we show that TNF alpha, in a
dose-dependent fashion, can potently inhibit the growth of primitive high
proliferative potential colony-forming cells (HPP-CFCs) stimulated by
multiple cytokine combinations. Using agonistic antibodies to the p55 and
p75 TNF receptors or TNF alpha mutants specific for either of the two TNF
receptors, we show that both receptors can mediate this inhibition. In
contrast, the potent stimulation of interleukin-3 (IL-3) plus
granulocyte-macrophage colony- stimulating factor (GM-CSF) induced HPP-CFC
colony formation observed at low concentrations of TNF alpha (2 ng/mL) was
only a p55-mediated event. Moreover, the stimulatory effects of TNF alpha
on GM-CSF or IL-3- induced colony formation, as well as the inhibition of
G-CSF-induced colony growth, were also exclusively signaled through the p55
TNF receptor. Taken together, our results suggest that the inhibitory
effects of TNF alpha on primitive bone marrow progenitor cells are mediated
through both p55 and p75 TNF receptors, whereas the p55 receptor
exclusively mediates the bidirectional effects on more mature, single
factor-responsive bone marrow progenitor cells as well as stimulation of
IL-3 plus GM-CSF-induced HPP-CFC colony growth.
Volume 83,
Issue 11,
pp. 3152-3159,
06/01/1994
Copyright © 1994 by The American Society of Hematology
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