Granulocyte colony‐stimulating factor administration modulates the surface expression of effector cell molecules on human monocytes

Abstract

Granulocyte colony‐stimulating factor (G‐CSF) has been shown to stimulate human neutrophil functions, both in vitro and in vivo. We examined the effects of G‐CSF administration on the surface expression of effector cell molecules on human neutrophils and monocytes. G‐CSF (50 μg/m2/d) was administered subcutaneously to five healthy volunteers once a day for 7 d. Venous blood was obtained immediately before and after 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 immunofluorescence using flow cytometry and monoclonal antibodies. The expression of CR1, CR3, FcRI and FcRII on neutrophils increased significantly after G‐CSF administration and then decreased after the last G‐CSF administration. The expression of human leucocyte adhesion molecule‐1 (LAM‐1) on neutrophils reflected the above expression. On the other hand, the administration of G‐CSF increased the expression of CR1, CR3, FcRI and FcRIII on monocytes. The expression of CR1, CR3 and FcRI on monocytes then decreased after the last G‐CSF administration, whereas the expression of FcRIII remained at an increased level. These findings indicate that G‐CSF administration modulates the expression of effector cell molecules 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.

G-CSF-induced decrease of the anti-granulocyte autoantibody levels in a patient with autoimmune granulocytopenia

“…The level of FcgRI and FcgRII expression gradually decreased after discontinuation of G-CSF. The events are in line with those observed in healthy G-CSF-treated volunteers [5,11,17]. Normal granulocytes also express FcgRIII (CD16) on their surface.…”

“…Normal granulocytes also express FcgRIII (CD16) on their surface. Other than in healthy volunteers [17], during treatment with repeated G-CSF injections we noted a significant and gradual increase in the FcgRIII expression that persisted for at least 3 days after discontinuation of G-CSF. The activation markers CD11b and CD66b followed the same pattern.…”

Recombinant Human Granulocyte Colony‐stimulating Factor and Neutrophil Phenotype

“…In a recent paper (Ohsaka et al, 1995), interesting data were stimulating factor (rhG-CSF) administration on circureported concerning the phenotypical changes that can be lating neutrophils and monocytes. caused by recombinant human granulocyte colonyAs far as neutrophils are concerned, the reported increase in FcRII (CD32) expression appears to be of particular interest, also because this finding is in agreement with very recent observations from our laboratory (Carulli et al, 1995).…”

Pyoderma Gangrenosum Following Cytosine Arabinoside, Aclarubicin and Granulocyte Colony-Stimulating Factor Combination Therapy in Myelodysplastic Syndrome.

“…Our previous studies indicated that G-CSF enhances O2~-release and modulates the surface expression of effector cell molecules on humanneutrophils in vivo (8,9). Wealso reported that G-CSF enhances O2~-release in neutrophils from MDSpatients both in vitro and in vivo (5).…”