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Free access | 10.1172/JCI105800
Arthritis Unit, the Department of Medicine, University of Minnesota College of Medicine, University Hospitals, Minneapolis, Minnesota 55455
Department of Pediatrics, University of Minnesota College of Medicine, University Hospitals, Minneapolis, Minnesota 55455
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Arthritis Unit, the Department of Medicine, University of Minnesota College of Medicine, University Hospitals, Minneapolis, Minnesota 55455
Department of Pediatrics, University of Minnesota College of Medicine, University Hospitals, Minneapolis, Minnesota 55455
Find articles by Laxdal, T. in: JCI | PubMed | Google Scholar
Arthritis Unit, the Department of Medicine, University of Minnesota College of Medicine, University Hospitals, Minneapolis, Minnesota 55455
Department of Pediatrics, University of Minnesota College of Medicine, University Hospitals, Minneapolis, Minnesota 55455
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Arthritis Unit, the Department of Medicine, University of Minnesota College of Medicine, University Hospitals, Minneapolis, Minnesota 55455
Department of Pediatrics, University of Minnesota College of Medicine, University Hospitals, Minneapolis, Minnesota 55455
Find articles by Williams, R. in: JCI | PubMed | Google Scholar
Published May 1, 1968 - More info
The effect of anti-γ-globulin factors on 7S γ-globulin opsonins from patients with subacute bacterial endocarditis has been examined with a quantitative in vitro phagocytosis system. Human anti-γ-globulin factors from patients with subacute bacterial endocarditis and rheumatoid arthritis inhibited the opsonic action of 7S γ-globulin specifically bound to bacteria. A similar antiopsonic effect was obtained with rabbit antiserum to human γG globulin. The antiopsonic effect of anti-γ-globulin factors did not correlate with their ability to potentiate agglutination of bacteria by 7S antibody. Competition was demonstrated between the antiopsonic effect of anti-γ-globulin factors and the phagocytosis-promoting action of heat-labile serum factors containing hemolytically active complement.