Interleukin 1 beta and the stimulation of Langerhans cell migration: comparisons with tumour necrosis factor alpha.

Abstract

Epidermal Langerhans cells (LC) and the cells into which they mature are believed to play a pivotal role in cutaneous immune function. The induction phase of contact sensitization is associated with the migration of LC from the skin and their accumulation as dendritic cells (DC) in lymph nodes draining the site of exposure. We have demonstrated previously that tumour necrosis factor alpha (TNF-alpha), an epidermal cytokine produced by keratinocytes, provides one signal for LC migration. We describe here experiments designed to evaluate the influence of interleukin 1 beta (IL-1 beta), a product exclusively of LC in murine epidermis, on LC migration, LC morphology and DC accumulation, and to compare the effects of this cytokine with those of TNF-alpha. Both cytokines induced a significant reduction in the frequency of epidermal LC and the arrival of DC in draining lymph nodes. Changes in both parameters were induced more rapidly following intradermal administration of TNF-alpha than were observed after treatment with IL-1 beta. However, the reduction in LC frequency was more persistent with IL-1 beta. Both cytokines caused the activation of LC, characterized by the acquisition of a more dendritic morphology and the increased expression of Ia molecules. These results demonstrate that IL-1 beta and TNF-alpha can each stimulate the migration of epidermal LC, but that the changes induced by these cytokines are not identical.