We have recently reported a series of experimental studies demonstrating certain genetic requirements for optimal thymus-derived-bone marrow-derived (T-B)2 cell cooperative interactions in the development of antibody responses to hapten-protein conjugates (1–4). Briefly, these studies have shown that in order for optimal physiologic, i.e., antigen-specific, T-B cell cooperation to occur, the interacting cells must share certain genes located in the histocompatibility gene complex. The experimental system employed in these studies was designed specifically to eliminate nonspecific T cell influences, of either an enhancing or suppressing nature, from the potential development of an “allogeneic effect” (reviewed in Reference 5). Indeed, in our initial attempts to investigate this problem, we found that adoptive transfer of spleen cells from donor mice primed to 2,4-dinitrophenyl (DNP)-keyhole limpet hemocyanin (KLH) into unprimed x-irradiated histoincompatible recipients resulted in nonspecific enhancement of anti-DNP antibody responses after challenge with a heterologous DNP-protein conjugate (1).

1

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

2

Abbreviations used in this paper: T, thymus, derived; B, bone marrow-derived; DNP, 2,4-dinitrophenyl; KLH, keyhole limpet hemocyanin; BGG, bovine γ-globulin; CFA, complete Freund's adjuvant.

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