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Interferon-gamma enhances factor-dependent myeloid proliferation of human
CD34+ hematopoietic progenitor cells
C Caux, I Moreau, S Saeland and J Banchereau
Schering-Plough, Laboratory for Immunological Research, Dardilly, France.
Numerous studies have shown that interferon-gamma (IFN gamma) inhibits the
proliferative effects of colony-stimulating factors (CSFs) on human bone
marrow cells. In the present study we investigated the effects of IFN gamma
and other described inhibitory factors on the proliferation of highly
purified CD34+ human hematopoietic progenitor cells (HPC) in response to
recombinant CSFs. While transforming growth factor-beta (TGF beta) and IFN
alpha were highly inhibitory, IFN gamma strongly potentiated interleukin-3
(IL-3) and, to a lesser extent, granulocyte- macrophage-CSF (GM-CSF)
induced growth of CD34+ HPC. IFN gamma had no significant proliferative
effect per se, and did not affect granulocyte- CSF (G-CSF)-dependent cell
proliferation. Within 10 days the number of viable cells generated in the
presence of IL-3 + IFN gamma was two times higher than in the presence of
IL-3 alone. Limiting dilution analysis showed that IFN gamma acts directly
on its target cell to increase the frequency of IL-3-responding cells
without affecting the average size of the IL-3-dependent clones. Enhanced
frequency of IL-3- and GM-CSF-responding cells was also observed in colony
assays where the addition of IFN gamma increased by twofold to threefold
the number of granulocyte colony-forming units (CFU-G), macrophage CFUs
(CFU-M), granulocyte-macrophage CFUs (CFU-GM), and mixed erythroid (E-MIX).
In contrast, IFN gamma did not affect the generation of erythroid burst-
forming units (BFU-e) in such cultures. In longer-term culture, the
combination of IFN gamma and IL-3 did not alter the lineage distribution of
the cells when compared with IL-3 alone. However, after 15 days, when
mature cells were present in the cultures, IFN gamma displayed cell
concentration-related growth-inhibitory effects. Thus, IFN gamma appears to
stimulate the early stage of myelopoiesis by enhancing the frequency of
growth factor-responding cells but, unlike tumor necrosis factor alpha (TNF
alpha), does not alter cell differentiation.
Volume 79,
Issue 10,
pp. 2628-2635,
05/15/1992
Copyright © 1992 by The American Society of Hematology
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