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The Journal of Immunology, 1972, 108: 34-44.
Copyright © 1972 by The American Association of Immunologists, Inc.
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Blocking of Autologous and Homologous Leukocyte Responses by Human Alloimmune Plasmas: A Possible in Vitro Correlate of Enhancement1

Rebecca H. Buckley, Richard I. Schiff2 and D. Bernard Amos

From the Departments of Pediatrics and Microbiology and Immunology, Duke University Medical Center, Durham, North Carolina 27710

Abstract

Four alloimmune plasmas were found to block the responses of autologous and many homologous lymphocytes to a variety of stimulants, including: phytohemagglutinin P (PHA-P), pokeweed mitogen (PWM), candida antigen, and mitomycin-C-treated allogeneic cells. Three of the plasmas contained lymphocytotoxic activity against the majority of leukocytes in cell panels selected to contain all known HL-A antigens. No cytotoxicity was present in the plasmas against lymphocytes of the plasma donors. The plasmas contained no detectable antibodies to PHA-P and PWM, and candida agglutinin titers were no higher in the blocking plasmas than in non-blocking control plasmas. The blocking of autologous responses by a given plasma showed no correlation with the HL-A types of allogeneic stimulator cells, and no apparent relationship to HL-A type was found in the ability of such a plasma to block homologous cell responses. The blocking was fully effective after heating the plasma to 56°C for 30 min. The effect on homologous responding cells was shown to be reversible, in that such cells could respond to PHA-P and candida antigen if they were washed after a 24-hr incubation period in blocking plasma and then resuspended in media containing autologous plasma. Both the blocking and cytotoxic activities were greatest in pure IgG fractions of the three plasmas that contained both activities. The data are most compatible with a direct inhibitory effect of the blocking plasmas on the responding cells rather than an antigen-masking effect.

Footnotes

1 This work was aided by grants from the National Foundation, the National Institute of Allergy and Infectious Disease (AI-10,15701), and the General Clinical Research Centers Program of the Division of Research Resources, National Institutes of Health (RR-30).

2 M.D.-Ph.D. candidate, trainee of the National Institutes of Health, National Institute of General Medical Sciences (T5-GM-1678).






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