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Tumor necrosis factor (TNF)-alpha directly inhibits human erythropoiesis in
vitro: role of p55 and p75 TNF receptors
LS Rusten and SE Jacobsen
Department of Immunology, Institute for Cancer Research, Norwegian Radium
Hospital, Oslo.
Two tumor necrosis factor receptors (TNFRs) with molecular weights of 55 kD
(TNFR-p55) and 75 kD (TNFR-p75) have recently been identified and cloned.
In previous studies, TNFR-p55 has been shown to exclusively mediate
bidirectional effects of TNF-alpha on committed bone marrow
granulocyte-macrophage progenitor cells, whereas both TNFR-p55 and TNFR-
p75 can mediate inhibition of primitive progenitors requiring multiple
cytokines to proliferate. We show here that TNF-alpha potently and directly
inhibits the in vitro growth of committed erythroid progenitor cells in
response to multiple cytokine combinations, and that TNF-alpha- induced
inhibition of burst-forming unit-erythroid colony formation is mainly
mediated through TNFR-p55, although TNFR-p75-mediated inhibition could be
observed on progenitors responsive to erythropoietin alone. Moreover, at
low TNF-alpha concentrations (2 ng/mL), TNF-alpha stimulates
interleukin-3-dependent in vitro growth of committed granulocyte-macrophage
progenitor cells, whereas it potently inhibits erythroid progenitor cell
proliferation, showing that one concentration of TNF-alpha can
simultaneously and bidirectionally modulate interleukin-3-dependent growth
of committed granulocyte-macrophage (stimulation) and erythroid progenitor
cells (inhibition).
Volume 85,
Issue 4,
pp. 989-996,
02/15/1995
Copyright © 1995 by The American Society of Hematology
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