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Decreased Fc and C3 receptor function in macrophage populations which are refractory to migration inhibitory factor,
Abstract:
Guinea pig macrophage populations previously established to be either responsive or refractory to activation by migration inhibitory factor (MIF) and Lotus fucolectin in the macrophage migration inhibition (MMI) assay were further characterized for their MMI response to diverse effectors as correlated with their Fc and C3b receptor function. MIF-refractory populations were found to be uniformly unresponsive to the complement activators: bacterial lipopolysaccharide, cobra venom factor, zymosan, and immune complex. MIF-responsive macrophages were responsive to the same activators. Fc-mediated binding and phagocytosis of IgG-coated sheep erythrocytes (EA) were markedly depressed in freshly harvested refractory macrophages as compared to responsive cells. Fc phagocytosis by refractory populations increased rapidly during 24-28 hr in vitro culture to levels equal to that of responsive cells which corresponded with an increase in their MMI response to MIF. Refractory macrophages also had decreased C3b receptor function as shown by reduced binding and phagocytosis of EAC or serum-coated zymosan and displayed a greater loss in C3b binding capacity than responsive cells during 48 hr in vitro culture. Trypsinization of responsive macrophages rendered them refractory in their MMI response to the various activators and selectively reversed C3b-dependent binding without effect on Fc binding. The plasmin esterase inhibitors, epsilon-amino-n-caproic acid, tranexamic acid, and L-lysine, previously established to reverse the MMI response to MIF, FBP, and C3 activators were found to inhibit both Fc- and C3-dependent phagocytosis. These results indicate that macrophage populations which are refractory to migration inhibition by MIF and C3 activators also have reduced Fc- and C3b-mediated phagocytic functions as compared to more mature responsive populations.
Insights
Guinea pig macrophages refractory to migration inhibitory factor (MIF) also show reduced Fc and C3b receptor function. These findings highlight the link between macrophage activation states and phagocytic capabilities.
Area of Science:
- Immunology
- Cell Biology
Background:
- Macrophage populations exhibit varying responsiveness to stimuli like migration inhibitory factor (MIF).
- Fc and C3b receptors are crucial for macrophage phagocytosis and immune responses.
Purpose of the Study:
- To characterize MIF-refractory and responsive guinea pig macrophage populations.
- To correlate macrophage migration inhibition (MMI) responses with Fc and C3b receptor function.
Main Methods:
- Macrophage migration inhibition (MMI) assay using diverse effectors.
- Assessment of Fc-mediated (IgG-coated erythrocytes) and C3b-mediated (serum-coated zymosan) phagocytosis.
- In vitro culture and trypsinization of macrophages.
Main Results:
- MIF-refractory macrophages were unresponsive to complement activators and showed depressed Fc and C3b receptor-mediated phagocytosis.
- In vitro culture increased Fc phagocytosis and MMI response in refractory macrophages.
- Trypsinization of responsive macrophages induced refractoriness and selectively impaired C3b binding.
- Plasmin esterase inhibitors affected both Fc- and C3-dependent phagocytosis.
Conclusions:
- Macrophage populations refractory to MIF and C3 activators exhibit diminished Fc and C3b-mediated phagocytic functions.
- Macrophage maturity correlates with responsiveness and receptor function.
- Fc and C3b receptor-mediated functions are linked to macrophage activation states.