Regulation of chemokine-mediated leukocyte migration within inflammatory tissues is a complex event that cannot be mimicked and analyzed in vitro.Hapten-induced contact hypersensitivity (CHS) is a highly frequent, often occupationally related human skin disorder in industrialized countries with an enormous sociomedical impact. 1 Moreover, CHS is considered as a standard model for an antigen-specific, T-lymphocytemediated immune response. 2 This concept still holds true for the clinically nonapparent sensitization phase of CHS with antigen-processing and presentation by Langerhans cells and a consecutive T cell stimulation in the draining lymph node. However, there is increasing evidence that during the clinically visible and physically disturbing elicitation phase of CHS nonspecific hapten-induced proinflammatory effects precede or parallel the antigen-specific effect and are a conditio sine qua non for the vigorous inflammatory reactions. 2 In a mouse CHS model Grabbe and colleagues 3 demonstrated that nonspecific effects of epicutaneously applied haptens contribute to the elicitation of CHS. Proinflammatory irritative rather than antigen-specific properties of the hapten are furthermore responsible for the strict concentration-dependence of the effector phase of CHS. Therefore, it is tempting to speculate that such irritative properties of haptens promote inflammatory skin reactions via induction of proinflammatory cytokines, adhesion molecules, and chemoattractants. Accordingly, some contact allergens such as urushiol, the relevant hapten in poison ivy, and nickel sulfate have been demonstrated to directly induce inflammatory activation of keratinocytes resulting in expression of ICAM-1, interleukin (IL)-8, and/or tumor necrosis factor (TNF)-␣. 4 -6 In recent years, in particular chemokines have emerged as potent stimulators of effector cell accumulation and activation and are likely candidates to mediate leukocyte recruitment during elicitation of CHS. Since the description of IL-8 more than a decade ago, the supergene Supported by grants from the W. Sander-Stiftung (95.064.2) (to R. G.) and from the Deutsche Forschungsgemeinschaft (811/1-3) to M. G. M. G. and A. Trautmann contributed equally to this work.