GRANULOCYTE-COLONY-STIMULATING FACTOR ADMINISTRATION MODULATES THE SURFACE EXPRESSION OF EFFECTOR CELL MOLECULES ON HUMAN MONOCYTES
Citation
A. Ohsaka et al., GRANULOCYTE-COLONY-STIMULATING FACTOR ADMINISTRATION MODULATES THE SURFACE EXPRESSION OF EFFECTOR CELL MOLECULES ON HUMAN MONOCYTES, British Journal of Haematology, 89(3), 1995, pp. 465-472
Categorie Soggetti
Hematology
SICI code
0007-1048(1995)89:3<465:GFAMTS>2.0.ZU;2-Q
Abstract
Granulocyte colony-stimulating factor (G-CSF) has been shown to stimul
ate human neutrophil functions, both in vitro and in vivo. We examined
the effects of G-CSF administration on the surface expression of effe
ctor cell molecules on human neutrophils and monocytes. G-CSF (50 mu g
/m(2)/d) was administered subcutaneously to five healthy volunteers on
ce a day for 7 d. Venous blood was obtained immediately before and aft
er the completion of G-CSF administration and 1 week after the last G-
CSF administration. The surface expression of complement receptors (CR
), Fc receptors for IgG (FcR) and cellular adhesion molecules on human
neutrophils and monocytes were determined by indirect immunofluoresce
nce using now cytometry and monoclonal antibodies. The expression of C
R1, CR3, FcRI and FcRII on neutrophils increased significantly after G
-CSF administration and then decreased after the last G-CSF administra
tion. The expression of human leucocyte adhesion molecule-1 (LAM-1) on
neutrophils reflected the above expression. On the other hand, the ad
ministration of G-CSF increased the expression of CR1, CR3, FcRI and F
cRIII on monocytes, The expression of CR1, CR3 and FcRI on monocytes t
hen decreased after the last G-CSF administration, whereas the express
ion of FcRIII remained at an increased level. These findings indicate
that G-CSF administration modulates the expression of effector cell mo
lecules on circulating monocytes as well as on neutrophils, resulting
in enhanced defence against selected infections or in potentiation of
the tumouricidal capacity of phagocytes in cancer patients.