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- Title
Regulation of macrophage Fc receptor expression and phagocytosis by histidine-rich glycoprotein.
- Authors
Chang, N.-S.; Leu, R. W.; Rummage, J. A.; Anderson, J. K.; Mole, J. E.
- Abstract
Regulation of macrophage Fc receptor (FcγR)-mediated phagocytic function by histidine-rich glycoprotein (HRG) was investigated. Pretreatment of oil-elicited inflammatory mouse peritoneal macrophages with HRG for 1-3 hr increased their FcγR-mediated binding and phagocytosis of IgG- opsonized sheep erythrocyte conjugates (EA). A significant reduction of FcγR-dependent EA binding and phagocytosis occurred after pretreatment of macrophages with HRG for more than 8 hr. These results indicate that HRG is capable of modulating FcγR expression in a biphasic fashion, which directly affects the overall efficiency of phagocytosis. HRG differentially regulated the functions of FcγR subclasses. For example, HRG reduced the efficiency of FcγRll (Fcγ2b/γlR)- dependent phagocytosis of erythrocytes conjugated with monoclonal IgG2b or lgG 1 by macrophages pretreated with URU for 24 hr. However, when similar studies were performed using erythrocytes coated with monoclonal IgG2a, HRG was less effective in inhibiting FcγRI (Fcγ2aR)- dependent phagocytosis. As an HRG-binding glycosaminoglycan. heparin failed to block the regulatory function of HRG on macrophages. Similarly, interferon-γ (IFN-γ) was not capable of blocking the functional activity of HRG. These studies suggest that HRG regulates macrophage function via a novel pathway different from that of heparin or IFN-γ.
- Subjects
MACROPHAGES; FC receptors; PHAGOCYTOSIS; GLYCOPROTEINS; GLYCOCONJUGATES; ANTIVIRAL agents
- Publication
Immunology, 1992, Vol 77, Issue 4, p532
- ISSN
0019-2805
- Publication type
Article