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Aplastic anemia: evidence for dysfunctional bone marrow progenitor cells
and the corrective effect of granulocyte colony-stimulating factor in vitro
J Scopes, S Daly, R Atkinson, SE Ball, EC Gordon-Smith and FM Gibson
Department of Cellular and Molecular Sciences, St. George's Hospital
Medical School, London, UK.
We investigated the effects of granulocyte-macrophage colony- stimulating
factor, interleukin-3, stem cell factor, interleukin-6, and granulocyte
colony-stimulating factor (G-CSF) alone, and in combination, on the
clonogenic potential of normal and aplastic anemia (AA) bone marrow
mononuclear cells (BMMC and CD34+ cells. AA BMMC consistently produced a
significantly lower absolute number of colonies than normal, but, when
account was taken of the reduced proportion of CD34+ cells in AA BM, there
was no significant difference in terms of cloning efficiency (CE). However,
when removed from the influence of accessory cells, the CE of AA CD34+
cells decreased significantly more than normal, indicating a defect in
their function, either in terms of dependence on accessory cell-derived
factors or susceptibility to cell damage when sorted. Of the factors
studied, G-CSF had the most significant effect on the response of CD34+
cells from both groups when removed from their accessory cells. This was
particularly true for AA CD34+ cells, whose response to cytokine stimuli
containing G-CSF enabled them to match the response of normal CD34+ cells.
Volume 87,
Issue 8,
pp. 3179-3185,
04/15/1996
Copyright © 1996 by The American Society of Hematology

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