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Ultraviolet‐B Radiation Upregulates Expression of Dectin‐2 on Epidermal Langerhans Cells by Activating the Gene Promoter ¶
Author(s) -
Bonkobara Makoto,
Yagihara Hiroko,
Yudate Tatsuo,
Chung JinSung,
Washizu Tsukimi,
Ariizumi Kiyoshi,
Cruz Ponciano D.
Publication year - 2005
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/j.1751-1097.2005.tb01467.x
Subject(s) - biology , microbiology and biotechnology , downregulation and upregulation , in vivo , gene expression , in vitro , antigen , gene , immunology , biochemistry
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 hyper‐sensitivity 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.