title: IL-10 augments CD23 expression on U937 cells and down-regulates IL-4-driven CD23 expression on cultured human blood monocytes: effects of IL-10 and other cytokines on cell phenotype and phagocytosis.
abstract: The effects of human recombinant interleukin-10 (IL-14) on the expression of several markers on U937 and human peripheral blood monocytes was studied by immunofluorescence and fluorescence-activated cell sorter (FACS) analysis. IL-10 augmented Fc IgE receptor (Fc epsilon RII/CD23) further enhanced by cotreatment with IL-4 or interferon-gamma (IFN-gamma). In contrast, the basal level of Fc epsilon RII expression on blood monocytes appeared to fall in response to IL-10, and this effect became more evident on IL-4-treated cells. Furthermore, the constitutive and IFN-gamma-triggered Fc gamma RI/CD64 expression was augmented on both monocytes and U937 cells. Thus the expression of Fc gamma RII/CD32, Fc gamma/RIII/CD16, Fc alpha R/CD89, the receptor for complement components (CR1/CD35, CD3/CD11b, CR4/CD11c) and the receptor for transferrin/CD71 was not significantly influenced on IL-10-treated cells. IL-10 modestly triggered CD14 antigen expression on monocytes but not U937. The expression of intercellular adhesion molecule-1 (ICAM-1)/CD54 on monocytes was significantly inhibited by IL-10. As expected, a marked reduction of the constitutive as well as of the IFN-gamma or IL-4-driven expression on HLA-DR, HLA-DP and HLA-DQ was observed on IL-10-cultured monocytes. On the other hand, the expression of major histocompatibility complex (MHC) class I molecules was slightly and dose-dependently induced on IL-10-treated monocytes. The ability of blood monocytes to phagocytose IgG-sensitized ox erythrocytes, and to bind and ingest opsonized Escherichia coli or latex particles, was amplified by IL-10. Our data demonstrate that IL-10 modulates the expression of a wide variety of structures on human mononuclear phagocytes, and augments their phagocytic capacity.
authors.affiliation: Institute of General and Experimental Pathology, University of Vienna, Austria.
authors.forename: A
authors.initials: A
authors.lastname: Spittler
authors.forename: C
authors.initials: C
authors.lastname: Schiller
authors.forename: M
authors.initials: M
authors.lastname: Willheim
authors.forename: C
authors.initials: C
authors.lastname: Tempfer
authors.forename: S
authors.initials: S
authors.lastname: Winkler
authors.forename: G
authors.initials: G
authors.lastname: Boltz-Nitulescu
mesh_terms: D002460:Cell Line; D004306:Dose-Response Relationship, Immunologic; D015536:Down-Regulation; D005434:Flow Cytometry; D005455:Fluorescent Antibody Technique; D006682:HLA-DP Antigens / Q000276:immunology; D006683:HLA-DQ Antigens / Q000276:immunology; D006684:HLA-DR Antigens / Q000276:immunology; D006801:Humans; D016753:Interleukin-10 / Q000494:pharmacology*; D015847:Interleukin-4 / Q000378:metabolism*; D009000:Monocytes / Q000276:immunology*; D010587:Phagocytosis; D017455:Receptors, IgE / Q000276:immunology*
chemical_list: D006682:HLA-DP Antigens; D006683:HLA-DQ Antigens; D006684:HLA-DR Antigens; D017455:Receptors, IgE; D016753:Interleukin-10; D015847:Interleukin-4