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Expression of granulocyte colony-stimulating factor and granulocyte
colony-stimulating factor receptor genes in partially overlapping
monoclonal B-cell populations from chronic lymphocytic leukemia patients
A Corcione, MV Corrias, S Daniele, S Zupo, M Spriano and V Pistoia
Laboratory of Oncology, Scientific Institute G. Gaslini, Genova, Italy.
B lymphocytes were purified from the peripheral blood of 30 B-cell chronic
lymphocytic leukemia (B-CLL) patients and tested for the ability to produce
granulocyte colony-stimulating factor (G-CSF) in vitro. Fifteen
Staphylococcus aureus Cowan I (SAC)-stimulated, but not unstimulated,
B-cell suspensions produced G-CSF in short-term cultures. Accordingly,
G-CSF mRNA was detected only in SAC-stimulated B cells. Five CLL B-cell
fractions that released G-CSF following exposure to SAC were also incubated
with CD40 or anti-mu antibodies in the presence or absence of recombinant
(r) interleukin-2 (IL-2) or IL-4. The 5 cell suspensions produced G-CSF
only on culture with CD40 monoclonal antibody in combination with rIL-2 or
rIL-4. CD5+ B lymphocytes, which represent the normal counterparts of most
B-CLL proliferations, did not produce G-CSF under any of the above culture
conditions. G-CSF produced by leukemic B lymphocytes was biologically
active, because conditioned media of SAC-stimulated cells supported the in
vitro growth of myeloid colonies from normal bone marrow progenitors. The
colony stimulating activity of CLL B-cell supernatants was ascribed to both
G-CSF and granulocyte-macrophage colony stimulating factor. G-CSF receptors
(G- CSFRs) were detected on freshly isolated B lymphocytes from 7 of 11 B-
CLL patients; 5 of these cell suspensions produced G-CSF in culture,
whereas 2 did not. rG-CSF rescued 3 of the 7 G-CSFR+ cell fractions from
spontaneous apoptosis but had no effect on their in vitro proliferation.
Volume 87,
Issue 7,
pp. 2861-2869,
04/01/1996
Copyright © 1996 by The American Society of Hematology
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