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Down‐modulation of receptors for granulocyte colony‐stimulating factor on human neutrophils by granulocyte‐activating agents
Author(s) -
Nicola N. A.,
Vadas M. A.,
Lopez A. F.
Publication year - 1986
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041280320
Subject(s) - granulocyte colony stimulating factor receptor , receptor , granulocyte , granulocyte colony stimulating factor , granulocyte macrophage colony stimulating factor receptor , n formylmethionine leucyl phenylalanine , lipopolysaccharide , biology , colony stimulating factor , cell surface receptor , microbiology and biotechnology , immunology , chemistry , biochemistry , in vitro , chemotaxis , haematopoiesis , macrophage colony stimulating factor , genetics , stem cell , chemotherapy , macrophage
Purified human blood neutrophils were able to bind radioiodinated murine granulocyte‐colony‐stimulating factor (G‐CSF) in a specific manner. This factor has previously been shown to stimulate functional activities of human and murine neutrophilic granulocytes and to be functionally analogous to human‐derived CSFβ. The binding of 125 I G‐CSF to human neutrophils was competed for equally by unlabeled G‐CSF and CSFβ but not by other CSF's. Saturation analysis indicated that human neutrophils displayed about 700–1,500 receptors for G‐CSF/CSFβ per cell. Three other agents (N‐formyl‐methionine‐leucine phenylalanine, bacterial lipopolysaccharide, and human CSFα) known to activate neutrophils did not compete directly for G‐CSF binding sites but, in preincubation experiments at 37°C, were able to down‐modulate the expression of G‐CSF receptors on human neutrophils in a dose‐ and time‐dependent manner. This effect was specific since the same agents have been shown elsewhere to up‐regulate the expression of other granulocyte surface antigens and other agents were much less effective at down‐modulating G‐CSF receptors. Since the granulocyte‐activating agents increase the sensitivity of human neutrophils to G‐CSF/CSFβ and mimic some of the actions of G‐CSF on neutrophils, it is suggested that G‐CSF receptor down‐modulation might be a mechanism whereby these agents activate G‐CSF receptors and thereby exert some of their effects.