Genetic regulation of delayed-type hypersensitivity responses to poly(LTyr,LGlu)-poly(DLAla)--poly(LLys). II. Evidence for a T-T-cell collaboration in delayed-type hypersensitivity responses and for a T-cell defect at the efferent phase in nonresponder H-2k mice.

The intercellular interactions and the site of the genetic defect in delayed-type hypersensitivity (DTH) response to poly(LTyr,LGlu)-poly(DLAla)--poly(LLys) [(T,G)-A--L] has been studied in a system where the T-cell education phase was separated from the efferent phase. In the cellular response, T-T-cell collaboration is required, because T cell-depleted mice were unable to manifest DTH responses after they were transferred with educated and irradiated T cells. Reconstitution of adult thymectomized mice that were irradiated and supplemented with bone marrow cells after treatment with anti-Thy-1.2 serum and complement, with T cells but not with accessory cells gave rise to significant responses. Educated, radioresistant cells required the presence of normal radiosensitive T cells for successful DTH responses to (T,G)-A--L. The genetic defect of nonresponder H-2k and H-2a mice has been located in the above-mentioned, second T-cell population that participates in the efferent phase of this immune reaction. Further characterization revealed that the educated cells are of the Lyt1+ phenotype and that the second normal T cells are expressing the Lyt 1+,2+,3+ phenotype. Thus, the genetic defect of H-2k and H-2a mice in the DTH response to (T,G)-A--L is expressed on the non-antigen-stimulated Lyt 1+,2+,3+ T cells.