Contact hypersensitivity (CHS) is an antigen-specific response elicited by exposure to certain low-molecularweight compounds termed haptens, and is the disease often seen clinically. CHS has also been used as a useful model to assess antigen-specific and T cell-dependent immune response. A wide variety of cells are thought to be involved in the pathogenesis of CHS. Keratinocytes and T cells are regarded as important factors, and besides these cells, mast cells, fibroblasts, B cells, macrophages, neutrophils have been demonstrated to be involved. From the studies of gene knockout experiments, it has been gleaned that IL-1β, IL-2, IL-3, IL-4, IL-6, IL-10, IFN-γ, TNF-α are associated with elicitation of CHS. While the roles of these cytokines in CHS have been well elucidated, recent attention has been directed at members of the superfamily of chemoattractant cytokines that are collectively termed chemokines. Both of mouse and human CHS studies showed chemokine genes were sequentially expressed in the elicitation site, suggesting that chemokine-mediated nonimmunological mechanisms precede and corroborate antigen-specific mechanisms during elicitation of CHS. In a mouse CHS study, topical treatment with a corticosteroid drug suppressed completely the infiltrates as well as the ear swelling response. In addition, the up-regulation of gene expressions for chemokines was suppressed by the corticosteroid drug, indicating that the expression of chemokine genes seems to be essential for orientating non-specific skin response to hapten-specific CHS response through the recruitment of inflammatory cells from the circulation into the tissue site. In this review, we discuss the proposed function of chemokines in the pathogenesis of CHS.