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The Journal of Immunology, 1974, 112: 926-934.
Copyright © 1974 by The American Association of Immunologists, Inc.

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Studies on the Induction and Expression of T Cell-Mediated Immunity

I. Blocking of Cell-Mediated Cytolysis by Membrane Antigens1

Benjamin Bonavida

Department of Microbiology and Immunology, University of California at Los Angeles, School of Medicine, Los Angeles, California 90024

Abstract

Serologically defined transplantation antigens from H-2b cells impaired the ability of immune BALB/c (H-2d) thymus-derived (T) cells to mediate cytolysis of 51Cr-EL-4 cells. The blocking antigens were obtained from either C57BL/6 spleens or EL-4 cells (both H-2b) by solubilization with 3 M KCl and by homogenization techniques. The blocking activity was specific and was not observed with immunologically unrelated histocompatibility antigens. Several characteristics of the blocking phenomenon were studied and revealed the following: 1) The blocking activity persisted if the immune cells were first exposed to the antigens and washed before admixing with the labeled target cells but was absent when the target cells were pretreated with the antigens. 2) Both spleens and educated T cells (from hydrocortisone-resistant thymocytes of BALB/c mice sensitized against H-2b cells) were inhibited by the transplantation antigens. These results established that antigen alone can block cell-mediated cytolysis at the effector level and rule out blocking by potential complexes formed by the antigen and de novo synthesized antibodies. 3) Blocking of cytolysis was dependent on the concentration of the antigen used for inhibition. 4) Membrane preparations were more inhibitory than equivalent concentration of soluble antigen. 5) Blocking was dependent on the length of the cytotoxic assay; more inhibition was observed in a 90-min assay than after 180 min of incubation. All of these findings indicate that specifically activated T lymphocytes have receptors for soluble alloantigens and T antigen interaction inhibits cytolysis of the corresponding target cells.

Footnotes

1 This work was supported by Grant CA 12800 from the National Cancer Institute, National Institutes of Health, Bethesda, Maryland.




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