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Blood, Vol. 94 No. 11 (December 1), 1999:
pp. 3764-3771
Altered Development and Cytokine Responses of Myeloid Progenitors in
the Absence of Transcription Factor, Interferon Consensus Sequence
Binding Protein
Marina Scheller,
John Foerster,
Clare M. Heyworth,
Jeffrey F. Waring,
Jürgen Löhler,
Gary L. Gilmore,
Richard K. Shadduck,
T. Mike Dexter, and
Ivan Horak
From the Abteilung für Molekulare Genetik, Forschungsinstitut
für Molekulare Pharmakologie, und Universitätsklinikum
Benjamin Franklin, Freie Universität Berlin, Berlin, Germany;
Heinrich-Pette Institut der Universität Hamburg, Hamburg,
Germany; Paterson Institute for Cancer Research, Manchester, UK; and
The Western Pennsylvania Cancer Institute, Pittsburgh, PA.
Mice deficient for the transcription factor, interferon consensus
sequence binding protein (ICSBP), are immunodeficient and develop
disease symptoms similar to human chronic myeloid leukemia (CML). To elucidate the hematopoietic disorder of
ICSBP / mice, we investigated the growth,
differentiation, and leukemogenic potential of ICSBP/
myeloid progenitor cells in vitro, as well as by cell-transfers in
vivo. We report that adult bone marrow, as well as fetal liver of
ICSBP-deficient mice harbor increased numbers of progenitor cells,
which are hyperresponsive to both granulocyte macrophage colony-stimulating factor (GM-CSF) and G-CSF in vitro. In contrast, their response to M-CSF is strongly reduced and, surprisingly, ICSBP/ colonies formed in the presence of M-CSF are
mostly of granulocytic morphology. This disproportional differentiation
toward cells of the granulocytic lineage in vitro parallels the
expansion of granulocytes in ICSBP/ mice and
correlates with a 4-fold reduction of M-CSF receptor expressing cells
in bone marrow. Cell transfer studies showed an intrinsic leukemogenic
potential and long-term reconstitution capability of
ICSBP/ progenitors. Further experiments demonstrated
strongly reduced adhesion of colony-forming cells from
ICSBP/ bone marrow to fibronectin. In summary,
ICSBP/ myeloid progenitor cells share several
abnormal features with CML progenitors, suggesting that the distal
parts of signaling pathways of these two disorders are overlapping.
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