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Tumor necrosis factor-alpha (TNF-alpha) potently enhances in vitro
macrophage production from primitive murine hematopoietic progenitor cells
in combination with stem cell factor and interleukin-7: novel stimulatory
role of p55 TNF receptors
C Fahlman, FW Jacobsen, OP Veiby, IK McNiece, HK Blomhoff and SE Jacobsen
Department of Immunology, Norwegian Radium Hospital, Montebello.
Tumor necrosis factor-alpha (TNF-alpha) is a bifunctional regulator of
hematopoiesis, and its cellular responses are mediated by two distinct cell
surface receptors. TNF-alpha generally inhibits the growth of primitive
murine hematopoietic progenitor cells (Lin-Scal+) in response to multiple
cytokine combinations, and the p75 TNF receptor is essential in signaling
such inhibition. In the present study we show the reverse phenomenon in
that TNF-alpha on the same progenitor cell population in combination with
stem cell factor (SCF) and interleukin-7 (IL-7) through the p55 TNF
receptor can recruit additional progenitors to proliferate. In contrast,
TGF-beta 1, another bifunctional regulator of hematopoietic progenitor cell
growth, completely blocked SCF plus IL- 7-induced proliferation. TNF-alpha
increased the number of responding progenitors, as well as the size of the
colonies formed. The synergistic effects of TNF-alpha were seen at the
single cell level, suggesting that its effects are directly mediated.
Finally, whereas SCF plus IL-7 promoted primarily granulopoiesis, the
addition of TNF-alpha switched the differentiation toward the production of
almost exclusively macrophages.
Volume 84,
Issue 5,
pp. 1528-1533,
09/01/1994
Copyright © 1994 by The American Society of Hematology
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