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Inhibition of the induction of contact hypersensitivity by a UV-mediated epidermal cytokine.

UVB exposure (290-320 nm) of mice has been shown to cause systemic suppression of contact hypersensitivity (CHS). Because UVB radiation hardly penetrates the epidermis, epidermal cells have been anticipated to be the site of the initiation of immunosuppression. Supernatants derived from UV-irradiated BALB/c epidermal cell cultures and a keratinocyte cell line (Pam 212) were evaluated for the ability to induce suppression of CHS after i.v. injection to BALB/c mice. Injection of supernatants derived from UV-treated epidermal cells and Pam 212 cells significantly blocked induction but not elicitation of CHS. In contrast, i.v. application of supernatants derived from unirradiated cells did not inhibit CHS. Using high-performance liquid chromatography gel filtration this mediator was shown to be a low-molecular-weight protein (15-50 kD). Moreover UV-mediated inhibitor production seems to be confined to epidermal cells since neither P 388 macrophages nor L 929 fibroblasts released this inhibitory cytokine. Therefore UV radiation may induce epidermal cells to produce an inhibitor of CHS which is distinct from prostaglandins and leukotrienes and may participate in the regulation of UV-mediated local as well as systemic immunosuppression.