The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation.
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-22Rα, the functional subunit of IL-22R, is mostly restricted to non-hematopoietic cell...
| Main Authors: | , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2017-01-01
|
| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC5448782?pdf=render |
| _version_ | 1818499606290366464 |
|---|---|
| author | Yejin Kim Junmyung Lee Jihoon Kim Chong Won Choi Young-Il Hwang Jae Seung Kang Wang Jae Lee |
| author_facet | Yejin Kim Junmyung Lee Jihoon Kim Chong Won Choi Young-Il Hwang Jae Seung Kang Wang Jae Lee |
| author_sort | Yejin Kim |
| collection | DOAJ |
| description | 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-22Rα, 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-22Rα. This study investigated IL-22Rα expression and IL-22-mediated proliferation and pro-inflammatory cytokine production by UVB-irradiated keratinocytes. IL-22Rα was increased in HaCaT and primary human keratinocytes after UVB irradiation through the translocation of IL-22Rα from the cytosol to the membrane. This increase in the expression of IL-22Rα 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-1α, IL-6, and IL-18 in UVB-irradiated HaCaT cells and primary human keratinocytes. Finally, IL-22Rα expression was increased in UVB-irradiated human and mouse skin by immunohistochemistry. The increased expression of IL-22Rα 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. |
| first_indexed | 2024-12-10T20:31:47Z |
| format | Article |
| id | doaj.art-8f8ddadbb1d849df93578f78cd9a3d85 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-10T20:31:47Z |
| publishDate | 2017-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-8f8ddadbb1d849df93578f78cd9a3d852022-12-22T01:34:39ZengPublic Library of Science (PLoS)PLoS ONE1932-62032017-01-01125e017856710.1371/journal.pone.0178567The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation.Yejin KimJunmyung LeeJihoon KimChong Won ChoiYoung-Il HwangJae Seung KangWang Jae LeeRecent 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-22Rα, 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-22Rα. This study investigated IL-22Rα expression and IL-22-mediated proliferation and pro-inflammatory cytokine production by UVB-irradiated keratinocytes. IL-22Rα was increased in HaCaT and primary human keratinocytes after UVB irradiation through the translocation of IL-22Rα from the cytosol to the membrane. This increase in the expression of IL-22Rα 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-1α, IL-6, and IL-18 in UVB-irradiated HaCaT cells and primary human keratinocytes. Finally, IL-22Rα expression was increased in UVB-irradiated human and mouse skin by immunohistochemistry. The increased expression of IL-22Rα 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.http://europepmc.org/articles/PMC5448782?pdf=render |
| spellingShingle | Yejin Kim Junmyung Lee Jihoon Kim Chong Won Choi Young-Il Hwang Jae Seung Kang Wang Jae Lee The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation. PLoS ONE |
| title | The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation. |
| title_full | The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation. |
| title_fullStr | The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation. |
| title_full_unstemmed | The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation. |
| title_short | The pathogenic role of interleukin-22 and its receptor during UVB-induced skin inflammation. |
| title_sort | pathogenic role of interleukin 22 and its receptor during uvb induced skin inflammation |
| url | http://europepmc.org/articles/PMC5448782?pdf=render |
| work_keys_str_mv | AT yejinkim thepathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT junmyunglee thepathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT jihoonkim thepathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT chongwonchoi thepathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT youngilhwang thepathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT jaeseungkang thepathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT wangjaelee thepathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT yejinkim pathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT junmyunglee pathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT jihoonkim pathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT chongwonchoi pathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT youngilhwang pathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT jaeseungkang pathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation AT wangjaelee pathogenicroleofinterleukin22anditsreceptorduringuvbinducedskininflammation |