There is increasing evidence that interleukin 1beta (IL-1beta), a product in murine epidermis of Langerhans cells (LC) exclusively, contributes to the initiation and regulation of LC migration in response to skin sensitization. The hypothesis is that IL-1beta induces the production by keratinocytes of tumour necrosis factor alpha (TNF-alpha) which acts in a paracrine fashion on LC to provide one signal for migration. In addition, it is believed that IL-1beta acts in an autocrine fashion on LC to provide a second, TNF-alpha-independent, signal for the initiation of this response. The viability of this hypothesis is dependent upon the availability of appropriate membrane receptors. We describe therefore experiments designed to investigate the IL-1 receptor (IL-1R) status of keratinocytes, LC and lymph node dendritic cells (DC). Flow cytometric analyses of epidermal cell suspensions revealed at least 60% of LC positive for the type I IL-1R (IL-1RI). In contrast, only a small proportion of keratinocytes displayed surface IL-1RI, although high intracellular expression of this receptor could be detected either by flow cytometric analysis of cells permeabilized with saponin or by immunofluorescence microscopy. Expression of the type II IL-1R (IL-1RII) was detected at relatively low levels on both LC and keratinocytes. Interestingly, DC isolated from the lymph nodes of sensitized mice displayed upregulated expression of IL-1RI and lower levels of IL-1RII compared to LC. The conclusion drawn is that the IL-1R phenotype of LC and keratinocytes under resting conditions is consistent with the proposed contribution of IL-1beta to LC migration. Furthermore, the regulation of IL-1R expression by epidermal cells and DC will undoubtedly influence the development of cutaneous immune responses.