Ultraviolet B irradiation decreases CXCL10 expression in keratinocytes through endoplasmic reticulum stress

Ultraviolet radiation is one of the standard treatment selections for psoriasis. interferon (IFN)‐γ and IFN‐γ‐induced CXCL10, which are highly expressed by keratinocytes in psoriasis lesion, are therapeutic targets for psoriasis. In this study, we found that ultraviolet B (UVB) irradiation inhibited IFN‐γ signaling events, including STAT1 phosphorylation and induction of CXCL10 messenger RNA (mRNA) expression in keratinocytes. IFN‐γ‐induced expression of CXCL10 mRNA in HaCaT cells, a human keratinocyte cell line, and human epithelial keratinocytes were also inhibited by H2O2 or endoplasmic reticulum (ER) stress inducers. Conversely, a mixture of antioxidants, Trolox and ascorbic acid, and the ER stress inhibitor salubrinal partially counteracted the inhibitory effect of UVB on IFN‐γ‐induced CXCL10 mRNA expression in HaCaT cells. We also found that UVB and ER stress reduced IFN‐γ receptor 1 protein levels in the plasma membrane fraction of keratinocytes. These observations suggested that ER stress and the generation of reactive oxygen species are essential for the inhibitory effect of UVB on IFN‐γ‐induced CXCL10 mRNA in keratinocytes. Graphical Ultraviolet B (UVB) irradiation inhibited interferon‐γ signaling events, including induction of STAT1 phosphorylation and CXCL10 messenger RNA expression in keratinocytes. This phenomenon might be due to the inhibition of IFN‐γ receptor 1 protein localization to the plasma membrane via endoplasmic reticulum stress induced by UVB irradiation