UVB RADIATION INTERRUPTS CYTOKINE-MEDIATED SUPPORT OF AN EPIDERMAL-DERIVED DENDRITIC CELL-LINE (XS52) BY A DUAL MECHANISM

We have established long-term dendritic cell lines from the epidermis of newborn mice. These cell lines (XS series) proliferate maximally in response to granulocyte/macrophage-colony stimulating factor, as well as to CSF-1, which is produced by skin-derived NS fibroblast lines an d by keratinocytes (albeit in smaller amounts). The purpose of this st udy was to examine the impact of UVB radiation on CSF-1-mediated inter action of dendritic cells with fibroblasts and keratinocytes. Exposure of NS cells to UVB radiation (unfiltered FS20 sunlamp) decreased CSF- 1 production at mRNA and protein levels. Both changes occurred in a do se-dependent fashion, with 50 J/m(2) causing a significant reduction. UVB radiation also downregulated CSF-1 mRNA expression by Pam 212 kera tinocytes. UVB exposure of XS cells diminished the surface expression of CSF-1 receptors, with 50 J/m(2) causing a significant reduction. Th us, UVB radiation interrupts CSF-1-mediated cell-cell interaction by a dual mechanism: downregulating CSF-1 production and abrogating CSF-1 receptor expression. Importantly, granulocyte/macrophage-colony stimul ating factor receptor expression by XS cells was also inhibited by UVB radiation, once again, with 50 J/m(2) producing significant inhibitio n. We propose that the resulting CSF-1 deficiency in epidermal microen vironment and unresponsiveness by dendritic cells to relevant growth f actors may contribute to UVB-mediated loss of resident epidermal dendr itic cells (i.e., Langerhans cells) in skin.