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

Photochem Photobiol. Jul-Aug 2005;81(4):944-8. doi: 10.1562/2004-10-21-RC-349.


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.

MeSH terms

  • Animals
  • Bone Marrow Cells / cytology
  • Bone Marrow Cells / radiation effects
  • Dendritic Cells / radiation effects
  • Female
  • Gene Expression Regulation / radiation effects*
  • Langerhans Cells / physiology*
  • Langerhans Cells / radiation effects
  • Lectins, C-Type / genetics*
  • Mice
  • Mice, Inbred C3H
  • Mice, Inbred ICR
  • Promoter Regions, Genetic / radiation effects*
  • Ultraviolet Rays*


  • Lectins, C-Type
  • dectin-2, mouse