Granulocyte colony-stimulating factor-induced terminal maturation of human myeloid cells is specifically associated with up-regulation of receptor-mediated function and CD10 expression.

The acute promyelocytic leukemia cell line NB4 was differentiated by all-trans retinoic acid (ATRA), which enhanced the superoxide-producing capacity stimulated by the chemotactic peptide and phorbol ester in this cell line. Granulocyte colony-stimulating factor (G-CSF) by itself had no effect on NB4 cells but exerted additional enhancing effects on the respiratory burst activity in the presence of ATRA. This finding was not due to the induction of G-CSF receptor by ATRA, because NB4 cells expressed abundant G-CSF receptor with or without ATRA. Unlike ATRA, G-CSF enhanced superoxide release stimulated by the chemotactic peptide but not by phorbol ester. In addition, G-CSF but not ATRA attenuated cell death and enhanced survival during differentiation. Cell surface expression of the chemotactic peptide receptors CD33 and CD10 but not of CD11b and CD11c was up-regulated by ATRA plus G-CSF far more profoundly than by ATRA alone. Fundamentally identical but slightly different phenomena for the cell surface expression of CD33 and CD10 were observed in the normal human bone marrow mononuclear cells; G-CSF induced CD10 even in the absence of ATRA and down-regulated CD33 in normal cells. The present results indicate that G-CSF-induced terminal maturation of human myeloid cells is associated with up-regulation of receptor-mediated function and CD10 expression.