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The Journal of Immunology, 1972, 108: 1162-1171.
Copyright © 1972 by The American Association of Immunologists, Inc.

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Antibody Islet Forming-Cells: Localized Hemolysis Inhibition in Gel1

John S. Hege and Wallace V. Epstein

From the Rheumatic Disease Group, Department of Medicine, University of California, San Francisco, California

Abstract

Spleen cells from mice immunized with human {gamma} globulin (HGG) and goat erythrocytes coated with human Forssman hemolysin were imbedded in agar and incubated with complement. Generalized hemolysis occurred revealing islets of intact erythrocytes representing single spleen cells releasing anti-HGG antibody. Back-ground hemolysis was increased and islets were more distinct when the goat erythrocytes were incubated with a carbodiimide reagent before coating with hemolysin.

Secondary HGG immunization yielded 50-fold more islets than did primary immunization. When background hemolysis was incomplete both islets and hemolytic plaques could be observed. Human IgM immunization yielded many more islets, but fewer plaques, than did IgG immunization. Evidence from this work and from the works of others suggests that islet-forming cells release antibody directed specifically against human immunoglobulin M, while plaque formation is the result of IgG antibody directed against human immunoglobulin G. In a system in which anti-globulin antibody modulates immune hemolysis, the immunoglobulin classes of both antiglobulin and hemolysin determine whether islets or plaques will occur.

Footnotes

1 This study was supported by Grant AM 01229, National Institutes of Health, Bethesda, Maryland, and a grant from the Academic Senate Committee on Research, Grant #32 (1970/71) University of California, San Francisco.







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