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The Journal of Immunology, 1969, 102: 241-252.
Copyright © 1969 by The American Association of Immunologists, Inc.
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Two Mechanisms of Immunologically-Induced Injury to Rabbit Platelets1

Roger M. Des Prez and Richard E. Bryant2

From the Department of Medicine, Vanderbilt University, and the Veterans Administration Hospital, Nashville, Tennessee

Abstract

Platelet injury (release of platelet 5-hydroxytryptamine) that occurs when antigen and antibody are added to non-immune platelet-rich plasma has been compared and contrasted to platelet injury that occurs when preformed immune precipitates are used as the challenge. Platelet injury by large concentrations of immune precipitate is not inhibited by citrate, by anticomplementary concentrations of heparin or sodium chloride, or by prior pepsin digestion of the antibody from which the precipitates are prepared. Prior zymosan adsorption of plasma at 16°C in the presence of Na2H2EDTA inhibits the precipitate-platelet interaction.

Platelet injury produced by soluble antigen and antibody in non-immune platelet-rich plasma is inhibited by citrate, by anticomplementary concentrations of heparin and sodium chloride, and by prior pepsin digestion of the antibody. Prior zymosan adsorption of plasma at 16°C in the presence of Na2H2EDTA is, however, without effect.

It is postulated that platelet injury by immune precipitates in citrated plasma results from phagocytosis of the precipitates by platelets and does not require complement, that platelet injury by soluble antigen and antibody in heparinized plasma is a complement-dependent process, and that platelet injury by immune precipitates in heparinized plasma may involve both mechanisms.

Footnotes

Supported by Research Grants HE 08399, AI 03082 and AI 00323 from the National Institutes of Health, United States Public Health Service, and the Veterans Administration.

2 Clinical Investigator, Veterans Administration.






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