Interleukin (IL)-2 functions to promote, as well as down-regulate, expansion of antigen-reactive CD4⁺ and CD8⁺ T cells, but the role of IL-2 in hapten-specific CD8⁺ T cell priming for contact hypersensitivity (CHS) responses remains untested. Using enzyme-linked immunospot to enumerate numbers of hapten-specific CD4⁺ and CD8⁺ T cells producing IL-2 in hapten-sensitized mice, the number of IL-2-producing CD8⁺ T cells was tenfold that of CD4⁺ T cells. Hapten-primed D4⁺ T cells produced low amounts of IL-2 during culture with hapten-presenting Langerhans cells, whereas production by hapten-primed CD8⁺ T cells was fivefold greater. CD8⁺ T cells did not express CD25 during hapten priming, but treatment with anti-IL-2 or anti-CD25 monoclonal antibodies during hapten sensitization increased hapten-specific effector CD8⁺ T cells as well as the magnitude and duration of the CHS response. These results indicate that CD8⁺ T cells are the primary source of IL-2 and that this IL-2 is required for the function of a population of CD4⁺CD25⁺ T cells to restrict the development of the hapten-reactive effector CD8⁺ T cells that mediate CHS responses.