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Granulocyte-macrophage colony-stimulating factor induces the expression of
the CD11b surface adhesion molecule on human granulocytes in vivo
MA Socinski, SA Cannistra, R Sullivan, A Elias, K Antman, L Schnipper and JD Griffin
Division of Tumor Immunology and Medicine, Dana Farber Cancer Institute,
Boston, MA 02115.
The CD11b (Mol) molecule is a member of a family of surface glycoproteins
that are essential for adhesion-dependent granulocyte functions. Brief
exposure of granulocytes to human granulocyte- macrophage
colony-stimulating factor (GM-CSF) in vitro increases the surface
expression of CD11b and increases granulocyte adhesiveness. To assess the
possible in vivo significance of these observations we studied the effect
of GM-CSF on CD11b, CD11a (LFA-1), and CD11c (gp 150, 95) expression on
granulocytes from nine adult patients with sarcoma who were receiving
GM-CSF as part of a phase I trial. GM-CSF was administered as a continuous
infusion at a dose of 32 or 64 micrograms/kg/d. Granulocyte CD11b, CD11a,
and CD11c expression was determined by indirect immunofluorescence staining
of whole blood, thereby minimizing in vitro manipulation. A transient
leukopenia developed within 15 minutes of initiation of GM-CSF treatment
that was associated with a marked increase in the surface antigen density
of CD11b. A mean 1.7-fold increase (P = .001) in the percentage of CD11b-
positive granulocytes and a mean 2.1-fold increase (P = .002) in CD11b
surface antigen density was noted after 12 hours of treatment. No change in
CD11a or CD11c expression was observed over the first 12 hours. The level
of CD11b expression was followed in six patients for up to 5 days of
treatment with GM-CSF. Compared with the 12-hour value, three of six
patients showed a subsequent decrease in CD11b expression, two remained
constant, and one showed a continued increase in CD11b surface density.
Fluorescence-activated cell sorting of granulocytes into high- and
low-density CD11b-positive groups revealed a preponderance of immature
myeloid forms in the low-density CD11b fraction, which suggests that the
late decrease in CD11b expression in some patients may be related to a
greater proportion of circulating immature myeloid forms in the peripheral
blood. This study suggests that GM-CSF administered as a continuous
infusion rapidly upregulates the expression of granulocyte CD11b in vivo.
The influence of this phenomenon on in vivo granulocyte aggregation may be
clinically relevant with regard to the toxicity of GM-CSF and deserves
further investigation.
Volume 72,
Issue 2,
pp. 691-697,
08/01/1988
Copyright © 1988 by The American Society of Hematology
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