Human eosinophils and parasitic diseases--III. Beta-interferon increases eosinophil IgG-Fc receptor expression and capacity.
Eosinophilic granulocytes from the blood of patients with parasitic diseases were preincubated in the presence or absence of beta-interferon (beta-IFN). The number of cells bearing IgG-Fc receptors was determined by rosette formation with chicken erythrocytes coated with IgG antibodies. beta-IFN augmented the expression of IgG-Fc receptors on the cells within 1 h incubation. Treatment of beta-IFN with heat or acid did not abolish the activity. The doses of beta-IFN needed to induce the modulations of IgG-Fc receptors could also augment the eosinophil-mediated antibody-dependent cytotoxicity (ADCC) against chicken red blood cells which resulted most pronounced when the IgG antibodies were present in suboptimal amount. These data suggest the role of beta-IFN in the host resistance to parasitic diseases, mainly in the initial phases of parasitic infestation when the specific IgG antibody levels are very low.
D000920:Antibody-Dependent Cell Cytotoxicity; D004804:Eosinophils / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000378:metabolism; D066298:In Vitro Techniques; D007370:Interferon Type I / Q000494:pharmacology*; D010272:Parasitic Diseases / Q000276:immunology*; D011961:Receptors, Fc / Q000378:metabolism*; D017452:Receptors, IgG
D007074:Immunoglobulin G; D007370:Interferon Type I; D011961:Receptors, Fc; D017452:Receptors, IgG