title: IgA-mediated inhibition of human leucocyte function by interference with Fc gamma and C3b receptors.
abstract: The inhibitory effects of IgA from human colostrum, and IgA1 and IgA2 from human serum on the chemiluminescence (CL) response and phagocytosis of polymorphonuclear leucocytes (PML) to Staphylococcus epidermidis and the CL response to formylmethionyl-leucyl-phenylalanine (FMLP) were studied. The dose-dependent inhibition of the luminol-mediated CL response of human PML to the bacteria was observed in the presence of more than 0.1 mg/ml IgA from both colostrum and serum. The preincubation of PML with a solution of IgA enhanced the suppressive effect of IgA on the cells. Removal of IgA from the reaction mixture after preincubation resulted in recovery, with time, of the response of PML to the bacteria. The bacteria treated with IgA did not give rise to any inhibition of the response. The CL response of PML to FMLP was not affected by the presence of IgA in the reaction mixture. The decrease of phagocytic activity of PML in the presence of IgA resulted in a decrease of NADPH oxidase activity of PML after stimulation with the bacteria as compared with the absence of IgA. The effect of IgA on the receptors of Fc and C3b (CR1) on the surface of PML was measured by monitoring erythrocyte-antibody (EA) or erythrocyte-antibody-complement (EAC) rosette formation and by direct and indirect immunofluorescence techniques using anti-CR1 antibody and Fc-specific antibodies. The presence of IgA in the reaction mixture led to a quantitative decrease in CR1 and the ability to bind IgG to the surface of PML.
authors.affiliation: Department of Oral Microbiology, School of Dentistry, Nippon Dental University, Niigata, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Saito
authors.forename: C
authors.initials: C
authors.lastname: Kato
authors.forename: H
authors.initials: H
authors.lastname: Katsuragi
authors.forename: A
authors.initials: A
authors.lastname: Komatsuzaki
mesh_terms: D000943:Antigens, Differentiation / Q000276:immunology*; D003179:Complement C3b / Q000276:immunology; D004306:Dose-Response Relationship, Immunologic; D006801:Humans; D007070:Immunoglobulin A / Q000276:immunology*; D007074:Immunoglobulin G / Q000276:immunology; D008163:Luminescent Measurements; D009247:NADH, NADPH Oxidoreductases / Q000032:analysis; D019255:NADPH Oxidases; D009504:Neutrophils / Q000201:enzymology / Q000276:immunology*; D010587:Phagocytosis; D011453:Prostaglandins / Q000096:biosynthesis; D011951:Receptors, Complement / Q000276:immunology*; D017463:Receptors, Complement 3b; D011961:Receptors, Fc / Q000276:immunology*; D017452:Receptors, IgG; D012397:Rosette Formation; D013212:Staphylococcus epidermidis / Q000276:immunology
chemical_list: D000943:Antigens, Differentiation; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D011453:Prostaglandins; D011951:Receptors, Complement; D017463:Receptors, Complement 3b; D011961:Receptors, Fc; D017452:Receptors, IgG; D003179:Complement C3b; D009247:NADH, NADPH Oxidoreductases; D019255:NADPH Oxidases