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      Colony-stimulating factors and interferon-gamma differentially affect cell surface molecules shared by monocytes and neutrophils.

      Clinical and Experimental Immunology
      Antibodies, Monoclonal, Antigens, Surface, biosynthesis, Cells, Cultured, Colony-Stimulating Factors, pharmacology, Fluorescent Antibody Technique, Granulocyte-Macrophage Colony-Stimulating Factor, Growth Substances, Histocompatibility Antigens Class II, Humans, Interferon-gamma, Macrophage Colony-Stimulating Factor, Monocytes, drug effects, metabolism, Neutrophils, Receptors, Fc

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          Abstract

          Monocytes and neutrophils share a common progenitor and perform many similar functions, as reflected in the expression of several shared membrane molecules. We show here that such molecules can be independently regulated by the cytokines interferon-gamma (IFN-gamma) and the colony-stimulating factors (CSF) in the context of the cell type on which they are present. Thus, IFN-gamma causes neutrophils to express the high-affinity receptor for IgG, Fc gamma RI, which has been considered to be a monocyte-specific receptor. Although neutrophil Fc gamma RI never reaches the levels present on monocytes, it is induced more rapidly and by lower amounts of IFN-gamma than monocyte Fc gamma RI. Of the CSF, only macrophage (M) CSF has an effect which is to cause a decrease in expression of monocyte Fc gamma RI. Secondly, after culture monocytes express Fc gamma RIII which is constitutively expressed by neutrophils. Although neutrophil Fc gamma RIII can be readily modulated by IFN-gamma, granulocyte (G) CSF and granulocyte-macrophage (GM) CSF, these cytokines do not alter the low levels of monocyte Fc gamma RIII. Thirdly, expression of the gp55 protein recognized by CD14 monoclonal antibodies is decreased after exposure of monocytes to IFN-gamma. Neutrophils express low levels of CD14 and, in this case, IFN-gamma causes an increase in the CD14 antigen on these cells. Of all the molecules investigated, only HLA class II is confined to monocytes, with increases in expression induced by IFN-gamma but not by the CSF.

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