Abstract
Resident and oil-elicited inflammatory peritoneal macrophages (PMΦ) from competent C3HeB/FeJ and genetically deficient C3H/HeJ mice were characterized for their Fe receptor (FcR)-dependent binding, phagocytic and ADCC functions during in vitro differentiation under the influence of mouse recombinant interferon-γ (rIFN-γ), interferon-α/β (IFN-α/β) fetal bovine serum (FBS), or in serum-free medium. Freshly cultured resident PMΦ from C3HeB/FeJ mice had low levels of FcR-mediated phagocytosis in response to mouse monoclonal IgGγ2a, IgGγ2b or IgGγ1, opsonized sheep erythrocytes as compared to oil-elicited inflammatory PMΦ from the same strain. Resident PMΦ were uniformly upregulated in their FcR-dependent phagocytosis after 24-48h in vitro culture with FBS to levels approximating that of freshly cultured inflammatory PMΦ which were also further upregulated after 24h in vitro culture with FBS. Both resident and inflammatory PMΦ were upregulated largely by an autostimulatory process in that they increased their FcR-mediated phagocytosis in serum-free RPMI-1640 medium without the addition of rIFN-γ or IFN-α/β, although FBS further augmented FcR upregulation. A synergistic effect of FBS and rIFN-γ was required for total reconstitution of FcR-mediated phagocytosis of FcR-incompetent C3H/HeJ inflammatory PMΦ in that FBS or rIFN-γ alone only partially reconstituted FcR function, whereas in combination full reconstitution occurred. Thus, macrophages from competent C3HeB/FeJ mice were upregulated in their FcR-mediated functions largely by an autostimulatory process, presumably dependent on endogenous of IFN-β, whereas, genetically-deficient C3H/HeJ macrophages required exogenous rIFN-γ in combination with fetal bovine serum for synergistic reconstitution of FcR functions. The uniform upregulation of FcR-dependent effector functions in vitro appears to provide an efficient system for enhanced immune function during differentiation which may be applicable to in vivo situations.
Published Version
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