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The Journal of Immunology, 1974, 113: 974-983.
Copyright © 1974 by The American Association of Immunologists, Inc.

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Hapten-Specific IgE Antibody Responses in Mice

IV. Evidence for Distinctive Sensitivities of IgE and IgG B Lymphocytes to the Regulatory Influences of T Cells1

David H. Katz, Toshiyuki Hamaoka, Peter E. Newburger and Baruj Benacerraf

From The Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

Abstract

The studies presented in this paper were performed to compare the responses of B lymphocytes of the IgG and IgE classes, respectively, to relatively constant conditions of activated T cell participation in antibody production by these cells. Two systems were employed: a) regulation of antibody responses by a potent nonantigen-specific T cell influence provided by the reaction of allogeneic T cells with alloantigens on the surface of antigen-specific B cells ("allogeneic effect"); and b) induction of adoptive secondary cooperative anti-hapten antibody responses by administering hapten and carrier determinants on separate molecules. The data presented here demonstrate that the allogeneic effect, although providing a potent mechanism for stimulating IgG B lymphocytes, either fails to stimulate or suppresses IgE B cells under the same conditions. Furthermore, under circumstances where antibody responses are elicited by administering nonlinked hapten and carrier determinants, the evidence implies that IgE B cells can be stimulated to a greater extent than IgG B cells in conditions of limited T cell participation. Taken collectively, these data support the concept that differences observed in the degree of helper function for one or the other antibody class may reflect differences in sensitivities of IgE vs IgG B cells to the complex enhancing and suppressive regulatory influences of the same T cell populations rather than to the existence of different T cells for different immunoglobulin classes.

Footnotes

1 This investigation was supported by Grants AI-10630 and AI-09920 from the National Institutes of Health, United States Public Health Service.







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