Differential Modulation of Macrophage Membrane Markers by Interferon: Analysis of Fc and C3b Receptors, Mac-1 and Ia Antigen Expression

Vogel, Stefanie N.; English, K E; Fertsch, D; Fultz, M J

doi:10.1089/jir.1983.3.153

Cited by 51 publications

(19 citation statements)

References 15 publications

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“…Previous reports have indicated that interferons enhanced Fc-mediated phagocytosis by macrophages (25) and macrophage cell line (27). In this report, IFN-f clearly enhanced Fc-mediated phagocytosis by BDM-1, while it had no effect on phagocytosis by BDM-1W3 (Fig.…”

supporting

confidence: 60%

Opposite Effects of Bacterial Lipopolysaccharide on Fc-Receptor-Mediated Phagocytosis of Two Bone Marrow-Derived Macrophage Cell Lines, BDM-1 and BDM-1W3.

Ohki

Soejima

Kohashi

et al. 1991

Cell Struct. Funct.

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ABSTRACT. Wehave reported the isolation and characterization of three factor-dependent macrophage cell lines from bone marrow cells of C3H/HeNmice. Wehave since isolated a subclone, BDM-1W3, from one of these cell lines. We found previously that BDM-1W3has a different sensitivity to bacterial lipopolysaccharide (LPS) for growth than its parental cell line, BDM-1. In this report, we show that LPS inhibits BDM-1W3phago-cytosis of antibody-coated sheep erythrocytes (Fc-mediated phagocytosis), whereas it enhanced Fc-mediated phagocytosis by BDM-1. It was observed that a loss of Fc-receptor capacity parallels a loss of phagocytic activity in LPS-treated BDM-1W3cells. LPS stimulated phagocytosis of latex beads by BDM-1and BDM-1W3,suggesting that Fc-mediated phagocytosis and phagocytosis of latex beads differ in their regulatory mechanisms. WhenBDM-1cells were cultured with LPS, they underwent drastic morphological changes, whereas LPStreated BDM-1W3 cells did not change significantly. Gammainterferon enhanced FC-mediated phagocytosis by BDM-1,while it had no significant effect on that by BDM-1W3. These cell lines should be useful for studying signal transduction mechanismsin LPS-mediated macrophage activation.The phagocytic activity of mononuclear phagocytes is important in the defense of the body against a variety of invading microorganisms. It has been reported that macrophages prepared from mice treated with thioglycolate or LPShave an enhanced phagocytic activity (3, 13). In contrast, a decrease in phagocytosis by peritoneal macrophages from BCG-treated mice has been reported (ll, 14 A number of murine macrophage cell lines have been isolated and characterized. Their properties seem to rep-* To whomcorrespondence should be addressed.

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supporting

confidence: 60%

Opposite Effects of Bacterial Lipopolysaccharide on Fc-Receptor-Mediated Phagocytosis of Two Bone Marrow-Derived Macrophage Cell Lines, BDM-1 and BDM-1W3.

Ohki

Soejima

Kohashi

et al. 1991

Cell Struct. Funct.

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“…It may downregulate expression of Ia antigen and Mac-1 expression on Kupffer cells [13,38], prevent the secretion of reactive oxygen intermediates by these cells [23], and decrease cytochrome-P-450-dependent drug transformation in hepatocytes [2].…”

Section: Discussionmentioning

confidence: 99%

Endogeneous interferon α/β produced by murine Kupffer cells augments liver-associated natural killing activity

Werner‐Wasik

et al. 1989

Cancer Immunol Immunother

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Nonparenchymal liver cells from untreated C3HeB/FeJ mice, when incubated in medium containing-10% fetal bovine serum or portal serum, produced significant amounts of interferon alpha/beta (IFN alpha/beta). In contrast, other cell populations (spleen, mononuclear blood cells and peritoneal cells) from C3HeB/FeJ mice or nonparenchymal liver cells from other strains of mice (C3H/HeJ, germ-free C3H/HeN and C57Bl/6J) produced little or no detectable IFN in fetal bovine serum under the same culture conditions. The cells in the nonparenchymal liver cell population responsible for IFN alpha/beta production were adherent, phagocytic, silica-sensitive, carbonyl-iron-sensitive, and Thy1.2-, presumably Kupffer cells or resident liver macrophages. IFN alpha/beta production by cultured Kupffer cells was not observed if medium containing fetal bovine serum or portal serum was treated with polymyxin B or if Kupffer cells were cultured in serum-free medium. This suggested that small amounts of endotoxin in fetal bovine or portal serum stimulated Kupffer cells to produce IFN alpha/beta. Possibly, Kupffer cells are in a different state of activation/maturation than peritoneal and splenic macrophages since the sensitivity of resident Kupffer cells from C3HeB/FeJ mice to the stimulatory effects of endotoxin. The endogenous production of IFN alpha/beta by Kupffer cells from C3HeB/FeJ mice can augment liver-associated natural killer (NK) activity against YAC-1 cells (4h) and induce liver-associated cytotoxic activity, not restricted by the major histocompatibility complex, against NK resistant P815 mastocytoma cells (18 h).

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“…IFN-fl is a fibroblast and epithelial cellderived cytokine [16] that has been shown to inhibit cell growth [17] and downregulate the expression of some membrane antigens (i.e" la antigen, Mac-1 in macrophages and recep tor for C3b) [18,19], The action of IFN-a and IFN-P is mediated through a common type-1 IFN receptor [20,21], IFN-p is thought to have a similar action to IFN-a.…”

Section: Introductionmentioning

confidence: 99%

Interferon-Beta Prevents Antigen-Induced Bronchial Inflammation and Airway Hyperreactivity in Mice

Maeda

Musoh²,

Shichijo³

et al. 1997

Pharmacology

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The effects of IFN-β and prednisolone (Pred) on antigen-induced IgE antibody production, airway eosinophilia and airway hyperreactivity (AHR) were studied in ovalbumin-sensitized Balb/c mice. Three inhalations of antigen (ovalbumin) caused an increase in the number of eosinophils and lymphocytes in bronchoalveolar lavage fluid and AHR to acetylcholine with a significant elevation in the serum IgE level. IFN-β clearly inhibited the antigen-induced airway inflammation and AHR, but did not affect IgE antibody production. Pred inhibited antigen-induced IgE antibody production, airway inflammation and AHR to acetylcholine. In addition, IFN-β inhibited T-helper type 2 (Th2) cell clone (D10G4.1)-induced peritoneal eosinophilia in mice, but did not affect neutrophilia, whereas Pred inhibited D10G4.1-induced peritoneal eosinophilia and neutrophilia. These results suggest that IFN-β inhibits antigen-induced bronchial inflammation and AHR probably due to the inhibition of Th2-induced airway eosinophilia.

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Differential Modulation of Macrophage Membrane Markers by Interferon: Analysis of Fc and C3b Receptors, Mac-1 and Ia Antigen Expression

Cited by 51 publications

References 15 publications

Opposite Effects of Bacterial Lipopolysaccharide on Fc-Receptor-Mediated Phagocytosis of Two Bone Marrow-Derived Macrophage Cell Lines, BDM-1 and BDM-1W3.

Opposite Effects of Bacterial Lipopolysaccharide on Fc-Receptor-Mediated Phagocytosis of Two Bone Marrow-Derived Macrophage Cell Lines, BDM-1 and BDM-1W3.

Endogeneous interferon α/β produced by murine Kupffer cells augments liver-associated natural killing activity

Interferon-Beta Prevents Antigen-Induced Bronchial Inflammation and Airway Hyperreactivity in Mice

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