科研之友
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摘要
Recent studies show that IL-22, a cytokine produced by activated CD4(+) T cells and NK cells, plays a pathogenic role in acute and chronic skin diseases. While IL-22 is produced by immune cells, the expression of IL-22R alpha, the functional subunit of IL-22R, is mostly restricted to non-hematopoietic cells in organs such as the skin and pancreas. Although it is well known that ultraviolet B (UVB) radiation induces skin inflammation, there have been no reports regarding the effect of UVB on the expression of IL-22R alpha. This study investigated IL22R alpha expression and IL-22-mediated proliferation and pro-inflammatory cytokine production by UVB-irradiated keratinocytes. IL-22R alpha was increased in HaCaT and primary human keratinocytes after UVB irradiation through the translocation of IL-22R alpha from the cytosol to the membrane. This increase in the expression of IL-22R alpha was mediated by the PI3K/Akt pathway. Moreover, the suppression of keratinocyte proliferation by UVB irradiation was inhibited by treatment with IL-22. At the same time, IL-22 increased the production of IL-la, IL-6, and IL-18 in UVB-irradiated HaCaT cells and primary human keratinocytes. Finally, IL22R alpha expression was increased in UVB-irradiated human and mouse skin by immunohistochemistry. The increased expression of IL-22R alpha therefore promotes keratinocyte proliferation and pro-inflammatory cytokine production during UVB-induced skin inflammation, suggesting that UVB facilitates skin inflammation by increasing the responsiveness of keratinocytes to IL-22. This study provides a new insight into UVB-induced skin inflammation and the regulation of related inflammatory skin diseases.
- 出版日期2017-5-30
