Antigen-presenting cells in the induction of contact hypersensitivity in mice: evidence that Langerhans cells are sufficient but not required.

One explanation for the fact that certain genetically defined strains of mice prove to be resistant to effects of low dose ultraviolet B radiation on the induction of contact hypersensitivity is that ultraviolet B resistant mice possess a second pathway for antigen presentation through the skin--a pathway that is independent of epidermal Langerhans cells and beyond the reach of the damaging effects of ultraviolet B light. As a corollary, ultraviolet-B susceptible mice would be expected to be deficient in this pathway. Several experimental strategies were employed to determine whether Langerhans cells are required for the induction of contact hypersensitivity by epicutaneously applied hapten. The results reveal that tape-stripped skin supports the induction of contact hypersensitivity, whereas surgical excision of hapten-painted skin within 1 h of application fails to permit the development of contact hypersensitivity. Because the former selectively eliminates epidermal Langerhans cells while the latter deletes both Langerhans cells and dermal antigen-presenting cells, we conclude that either Langerhans cells or dermal cells are sufficient to provide antigen presentation in the induction of contact hypersensitivity. When large amounts of hapten are painted epicutaneously, or when hapten is injected subcutaneously or painted on sub-dermal tissues, contact hypersensitivity also results, indicating that induction of contact hypersensitivity does not require that antigen processing and presentation be provided by cutaneous cells. Reasons are presented for concluding that under physiologic circumstances induction of contact hypersensitivity by epicutaneous hapten application relies primarily upon the antigen-presenting capabilities of epidermal (Langerhans cells) and dermal cells.