When unprimed C57BL T cells were transferred into C57BL nu/nu mice, a preferential enhancement of the IgG2a antibody response to TNP-Ficoll was observed. Unprimed splenic T cells from Igh allotype congenic (B.C8) mice were unable to enhance the IgG2a response. The failure of T cells from allotype congenic mice to augment IgG2a antibody production to TNP-Ficoll was due to the presence of a T cell that specifically suppressed IgG2a antibody synthesis. The suppressive activity could be demonstrated in nu/nu mice and nu/nu mice reconstituted with C57BL helper cells. The suppressive activity of the B.C8 T cell population could be abrogated by treatment with anti-Lyt-1 and anti-Lyt-2 antibodies and complement as well as by treatment of B.C8 T cells with anti-Lyt-2 alone. Removal of the T cells responsible for IgG2a suppression from B.C8 splenic T cell population unmasked a population of B.C8 T cells that could enhance IgG2a preferentially augment IgG2a antibody synthesis can be found in donor mice that differ in their Igh background from the responding B cells.