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  • 1
    Electronic Resource
    Electronic Resource
    The Formyl Peptide N-Formyl-methionyl-leucyl-phenylalanine Downregulates the Expression of FcγRs in Interferon-γ-Activated Monocytes/Macrophages In Vitro and In Vivo (2003)
    Oxford, UK : Blackwell Science Ltd
    Scandinavian journal of immunology 57 (2003), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: N-Formyl peptides are cleavage products of bacterial and mitochondrial proteins that have pro-inflammatory activities and play an important role in antibacterial host defence. FcγRI is a receptor for the Fc portion of immunoglobulin G expressed in monocytes that mediates cytotoxicity and is upregulated by interferon-γ (IFN-γ) and interleukin-10 (IL-10). In this report, we demonstrate that N-formyl-methionyl-leucyl-phenylalanine (FMLP) downregulates the expression of FcγRI in IFN-γ-treated monocytes, but not in IL-10-treated monocytes. We determine that supernatants obtained from monocytes treated with IFN-γ and then exposed to FMLP induce the downregulation of FcγRI in naïve monocytes. This effect is abrogated by the protease inhibitors phenylmethylsulphonyl fluoride and phosphoramidon, which inhibit serine and metalloproteases, respectively. Supernatants from FMLP-treated neutrophils also induce the downregulation of FcγRI, when added to naïve monocytes. Similar observations were obtained in vivo in a mouse model of chronic inflammation. In vivo, FMLP also downregulates the expression of FcγRs in IFN-γ-activated macrophages. Our results support the existence of a new mechanism through which FMLP could modulate the activity of monocytes/macrophages during bacterial infections.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.2003.01219.x
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  • 2
    Electronic Resource
    Electronic Resource
    Anti-Oxidants Inhibit the Enhancement of the Immune Response Caused by Oil Adjuvants (1996)
    Oxford, U.K. and Cambridge, USA : Blackwell Science Ltd
    Scandinavian journal of immunology 43 (1996), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Adjuvants are agents that can induce strong immunity to different antigens. They are thought to act mainly by stimulating macrophages, causing the release of cytokines, which in turn induce an inflammatory focus necessary for the adjuvant action. The authors found that catalase, ascorbic acid, N-acetylcysteine and glutathione are able to inhibit the enhancing effect of incomplete Freund adjuvant (IFA) and polyoxyethylated castor oil upon the humoral immune response to sheep red blood cells (SRBC). None of the anti-oxidants tested inhibited the basal immune response to the antigen. In addition, mice inoculated with different concentrations of hydrogen peroxide showed an enhanced response against SRBC, mimicking the effect observed with adjuvants. Delayed type hypersensitivity induced by SRBC in the presence of IFA was also inhibited by catalase. In conclusion, the report indicates that oxygen radicals are crucial molecules involved in the adjuvant effect observed in SRBC immunized mice.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.1996.d01-59.x
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Interferon-Gamma Enhances PAF-Acether Production by Stimulated Human Polymorphonuclear Leucocytes (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 33 (1991), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Human polymorphonuclear leucocytes (PMN) stimulated with either immune complexes (IC), phorbol myristate acetate (PMA) or N-formyl-methionyl-leucyl-phenylalanine (FMLP) generate platelet-activating factor (PAF-acether), The present study demonstrates that treatment of PMN with recombinant human interferon-gamma (IFN-y) significantly enhanced the production of PAF-acether by stimulated cells, in a concentration-dependent mode. On the contrary, α and β IFN were completely unable to increase PAF-acether synthesis by stimulated PMN. The significance of these results is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1991.tb02528.x
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Neutrophil Cytotoxicity Induced by Immune Complexes prepared with Cationized Antibodies (1993)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 37 (1993), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Here we analyse the ability of soluble imtnune complexes (IC) prepared with cationized antibodies to induce cytotoxic responses mediated by neutrophils. While eationized IC induced high levels of cytotoxicity, control IC induced very low levels of response. Inhibition of cytotoxicity by catalase but not by three haemenzyme inhibitors suggests that oxygen-dependent but myeloperoxidase-independent mechanisms are responsible for cytolysis. While the response induced by control IC was enhanced by cytochalasin B and was not modified by colchicine, that induced by cationized IC was markedly inhibited by cytochalasin B and significantly enhanced by colchicine. Cytotoxicity induced by cationized IC was completely abrogated by monoclonal antibodies to FcγRII. Using control IC, a partial inhibition was observed employing either anti-FcγRII or anti-FcγRIII monoclonal antibodies. Treatment of neutrophils with ehemotrypsine or pronase significantly enhanced cytotoxicity induced by cationized IC but not by control IC. We also found that non-specific absorptive mechanisms appear to play an important role in the binding of cationized IC, but not control IC, to the neutrophil surface. The significance of these results is discussed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1365-3083.1993.tb01755.x
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    Paper (German National Licenses)
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