A single intraperitoneal injection of the monovalent synthetic antigen, tyrosinated trimethylaminoaniline [tyr(TMA)] in Freund's complete adjuvant induces an antiidiotypic second-order T suppressor (Ts2) cell population 6 wk later. This population was able to suppress TMA-specific delayed-type hypersensitivity (DTH) responses when adoptively transferred into normal syngeneic recipients. However, they failed to function intrinsically. The inability of the Ts2 to function intrinsically was not caused by compensating idiotype-negative T cells that mediate DTH. Rather, this paradoxical observation was found to be caused by the absence or loss of function of a critical modulatory T cell population in the suppressor cell-bearing mice. This cell is functionally active in normal mice immunized for DTH responses and is sensitive to cyclophosphamide treatment. In addition, this cell type bears idiotype on its surface and is Thy-1+ and Lyt-1-,2+. It was demonstrated that by adoptively transferring the activated modulatory T cells from normal mice into tyr(TMA)-immune recipients, it was possible to observe suppressor cell function intrinsically. The potential importance of modulatory T cell function in the regulation of antibody and DTH responses is discussed.

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