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Macrophage inflammatory protein-1 alpha receptors are present on cells
enriched for CD34 expression from patients with chronic myeloid leukemia
RC Chasty, GS Lucas, PJ Owen-Lynch, A Pierce and AD Whetton
Department of Biochemistry and Applied Molecular Biology, UMIST, Manchester
Royal Infirmary, UK.
The response of normal and chronic myeloid leukemia (CML), CD34+ cells to
human macrophage inflammatory protein-1 alpha (MIP-1 alpha or LD78) was
assessed. In tritiated thymidine incorporation assays, stem cell factor
plus granulocyte-macrophage colony-stimulating factor stimulated thymidine
incorporation in normal CD34+ cells was reduced to 72% of control values in
the presence of MIP-1 alpha, whereas incorporation by CML CD34+ cells
exposed to the same factors was not altered. In clonogenic assays, the
presence of MIP-1 alpha gave a level of colony formation that was 71% of
control values for normal progenitor cells, whereas for CML CD34+ cells
colony formation was enhanced by 25%. These results suggest that, in vitro,
CML progenitor cells are relatively refractory to the growth inhibitory
effects of MIP-1 alpha. Using flow cytometry, the specific binding of a
biotinylated human MIP-1 alpha/avidin fluorescein (FITC) conjugate to
normal and CML mononuclear and CD34+ cell populations was quantified. The
data indicate that (for both normal and CML CD34+ cells) there was a single
population of cells that express cell surface receptors for MIP-1 alpha and
this receptor expression was independent of cell cycle status. CML
progenitor cells may be refractory to the effects of MIP-1 alpha as a
result of events downstream from receptor expression.
Volume 86,
Issue 11,
pp. 4270-4277,
12/01/1995
Copyright © 1995 by The American Society of Hematology
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