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Human colony-stimulating factor 1 (CSF-1) receptor confers CSF-1
responsiveness to interleukin-3-dependent 32DC13 mouse myeloid cells and
abrogates differentiation in response to granulocyte CSF
J Kato and CJ Sherr
Howard Hughes Medical Institute, Department of Tumor Cell Biology, St Jude
Children's Research Hospital, Memphis, TN 38105.
Interleukin-3 (IL-3)-dependent mouse myeloid 32DC13 cells differentiate to
neutrophils in response to granulocyte colony-stimulating factor (G- CSF).
Introduction of the human c-fms gene, which encodes the receptor for CSF-1,
into 32DC13 cells gave rise to variants that were able to proliferate in
medium containing either murine IL-3 or human recombinant CSF-1, but were
unable to differentiate to granulocytes in response to G-CSF. Unlike
parental 32CD13 cells, CSF-1-responsive derivatives expressed nonspecific
esterase when grown in CSF-1, but did not exhibit many other morphologic,
immunologic, or functional properties of mononuclear phagocyte
differentiation, or express murine CSF-1 receptors. Accelerated turnover of
the human CSF-1 receptor was observed in response to CSF-1 and phorbol
esters, but not after stimulation with IL-3 or bacterial
lipopolysaccharide. Although both CSF-1 and IL-3 induced tyrosine
phosphorylation of heterologous substrates in the dually responsive cells,
differences in the patterns of substrate phosphorylation were observed in
response to the two hematopoietins. We conclude that expression of the
human CSF-1 receptor in 32DC13 cells not only induces CSF-1 responsiveness,
but alters its phenotype in a way that prohibits granulocyte
differentiation.
Volume 75,
Issue 9,
pp. 1780-1787,
05/01/1990
Copyright © 1990 by The American Society of Hematology
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