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The Journal of Immunology, 1974, 113: 1716-1725.
Copyright © 1974 by The American Association of Immunologists, Inc.

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Specific Suppression of Delayed Hypersensitivity: The Possible Presence of a Suppressor B Cell in the Regulation of Delayed Hypersensitivity1

Ruth Neta and S. B. Salvin

From the Department of Microbiology, University of Pittsburgh, School of Medicine, Pittsburgh, Pennsylvania 15261

Abstract

Delayed hypersensitivity to purified protein antigens in incomplete Freund's adjuvant is of a transient nature in guinea pigs. This decrease in delayed reactivity can be transferred adoptively to a sensitized recipient with lymphoid cells from the spleens and peritoneal exudate of donors 8 days after sensitization with ovalbumin. When such mixtures of donor lymphoid cells are adoptively transferred at subsequent times after sensitization, the delayed hypersensitivity of the recipient is not suppressed. When a hapten-protein conjugate, such as para-aminobenzoic acid-azo-hen egg albumin is used as a sensitizing antigen in the donor, and when the donor cells are removed at various time intervals after the decline in delayed skin tests to the carrier protein as antigen, such as 10 to 23 days after sensitization, adoptive transfer of lymphoid cells into sensitized recipients suppresses the elicitation of delayed skin hypersensitivity to the carrier. When spleen cells are compared with peritoneal exudate (PE) cells in their suppressive capacities, only the spleen cells show suppressive action. The duration of delayed responses varied inversely with the dose of the immunosuppressive drug in guinea pigs treated with varying doses of cyclophosphamide 72 hr before sensitization. In view of the observations that PE cells are an enriched source of T cells and that the particular schedule of treatment with cyclophosphamide affects rapidly dividing cells, the suggestion is made that a suppressor B cell may regulate the activity of a T cell in the expression of delayed skin hypersensitivity.

Footnotes

1 This investigation was supported by the United States-Japan Cooperative Medical Science Program administered by the National Institute of Allergy and Infectious diseases of the National Institutes of Health, Grant AI-08528 and also Grant AI-11945.







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