The factors mediating recruitment of immune T cells to challenge sites during contact hypersensitivity (CHS) responses remain unclear. To investigate the role of chemokines during elicitation of CHS, the temporal expression of chemokine genes in hapten-challenged ears was tested. KC (the murine homologoue of Groalpha) was expressed 30 min following hapten challenge in naive and hapten-sensitized mice. A rabbit KC-specific antiserum inhibited elicitation of CHS when administered to sensitized mice prior to hapten challenge. Injecting either neutrophils or immune CD8(+) T cells into the ear tissue of immune animals before hapten challenge circumvented the KC antiserum-mediated inhibition of CHS. Neutrophil depletion also inhibited CHS and was circumvented by injecting either neutrophils or hapten-primed CD8(+) T cells into ears of sensitized mice followed by specific hapten challenge. These results indicate that KC-directed neutrophil infiltration of hapten challenge sites is required for elicitation of CHS and suggest that neutrophils mediate recruitment of the hapten-specific CD8(+) T cells that subsequently produce cytokines mediating the hypersensitivity response.