AbstractSpecific antibody unresponsiveness was induced in adult CBA/H mice by the injection of cyclophosphamide 24 h after immunization with a large dose of horse red blood cells (HRBC). Four lines of experimental evidence indicated that this unresponsive state was maintained by active T cell repression. First, the cellular basis of the unresponsive state was in the T cell rather than the B cell population. Second, when normal spleen cells were transferred into the unresponsive animals, they were unable to break the unresponsive state. Third, the induction of unresponsiveness was antagonized by anti‐lymphocyte serum. Finally, T cells from unresponsive mice specifically repressed the anti‐HRBC antibody response of normal spleen cells when these were mixed together and injected into irradiated recipients.However, although the mice were unresponsive to HRBC at the humoral level, via active T cell repression, they simultaneously expressed high levels of delayed‐type hypersensitivity (DTH) to HRBC. In contrast, we have reported recently (Eur. J. Immunol.1976. 6: 674) that T cells from mice expressing humoral immunity to HRBC can specifically suppress the development of DTH to HRBC. On the basis of these two sets of observations, it is suggested that the frequently observed inverse relationship between humoral and cell‐mediated immunity is mediated by different types of inhibitory T cells. The role of T cell help in the induction of these different types of immunity is also di
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