Ultraviolet-B radiation upregulates expression of dectin-2 on epidermal Langerhans cells by activating the gene promoter.

Epidermal Langerhans cells (LC) belong to the antigen-presenting cell (APC) family of dendritic cells that can initiate antigen-specific immunogenic or tolerogenic responses. In mice, we have shown ultraviolet-B (UV-B) irradiation to induce long-lasting suppression (tolerance) of contact hypersensitivity responses by converting LC from immunogenic to tolerogenic APC. The C-type lectin receptor, dectin-2, expressed preferentially by LC and dendritic cells, has also been shown to be involved in inducing this form of UV-B-induced immunosuppression. These observations led us to question whether UV-B can modulate dectin-2 expression by LC. In ICR mice engineered to express the dectin-2 gene promoter linked to a luciferase reporter gene, we found broadband UV-B treatment in vivo to activate the promoter in LC. In wild-type C3H/HeN mice, we found such treatment in vivo to yield LC with increased dectin-2 expression at both mRNA and protein levels. Broadband UV-B treatment in vitro of bone marrow-derived dendritic cells from these mice also showed upregulated expression of dectin-2 mRNA. These findings lead us to conclude that broadband UV-B upregulates dectin-2 expression in LC by activating the dectin-2 gene promoter. Such amplification suggests that UV-B-induced immunosuppression may be due (at least in part) to augmented dectin-2 expression in LC.