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Cell Interactions Between Histoincompatible T and B Lymphocytes

IX. The Failure of Histoincompatible Cells Is Not Due to Suppression and Cannot Be Circumvented by Carrier-Priming T Cells with Allogeneic Macrophages¹

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

Abstract

Two possible explanations for the failure of primed histoincompatible T and B lymphocytes to cooperate in secondary responses of the IgG antibody class have been investigated in the present study: 1) The possible existence of subtle suppressive mechanisms developing as a consequence of mixing two histoincompatible cell populations; and 2) The possible inability of histoincompatible carrierprimed T cells to recognize and/or be induced to function by carrier determinants presented to them in association with foreign MHC antigens (i.e., the "altered-self" recognition hypothesis). Absence of suppression has been verified by two different approaches, including: 1) the failure of histoincompatible T cells, even in great excess, to interfere with physiologic cooperation between syngeneic T and B lymphocytes; and 2) the failure of histoincompatible B cells to interfere with physiologic cooperation between semi-syngeneic F₁ hybrid T cells and parental B cells. The unlikelihood of the "altered-self" explanation for failure of histoincompatible T and B cells to cooperate has been indicated by an inability to circumvent the requirement for I-region identity by priming T cells with allogeneic macrophagebound antigen even when the latter cells are of identical haploytpe with the allogeneic B cells employed in the final cooperation assay.

These results strongly substantiate the existence of true genetic restrictions in T-B cell intractions in secondary responses to hapten-protein conjugates. The validity of other observations indicating an absence of genetic restrictions in certain circumstances, considered in the context of our own data, has suggested the possibility that virgin T and B lymphocytes reciprocally influence one another during the course of cell interactions in response to antigenic and/or other signals, a process we term "adaptive differentiation."

Footnotes

¹ This work was supported by Grant AI-10630 from the National Institutes of Health, United States Public Health Service, Bethesda, Maryland.

² Present address: Department of Cellular and Developmental Immunology, Scripps Clinic and Research Foundation, 10666 North Torrey Pines Road, La Jolla, California 92037.

³ N. C. is supported by National Institutes of Health National Research Service Award 1-F32-AI-01965 from the National Institute of Allergy and Infectious Diseases. Present address: The Rockefeller University, New York, New York 10021.