Abstract 4900: The role of Interleukin (IL)-22 on the UVB-induced proliferation and inflammation of human keratinocyte cell line, HaCaT

Abstract

Abstract Interleukin 22 (IL-22), a member of IL-10 family, is a potent mediator of inflammatory responses. It is produced by activated CD4+ T cells and natural killer (NK) cells, but IL-22Rα expression is restricted to nonhematopoietic cells in the skin, pancreas, intestine, liver, lung and kidney. IL-22 suppresses IL-4 production from Th2 cells and induces acute phase proteins in liver and pancreas. It is recently found that IL-22 plays a critical role in the maintenance of epidermal homeostasis by controlling cell cycle of keratinocytes. Therefore, we investigated that role of IL-22 on the proliferation and inflammation of ultraviolet B (UVB)-irradiated human keratinocytes, HaCaT. First, we found the expression of IL-22Rα mRNA and protein level was increased in HaCaT by UVB (100 J/m2) irradiation. Interestingly, the translocation of IL-22Rα from cytosol to membrane was increased by UVB irradiation. When UVB-irradiated HaCaT was cultured in the presence of recombinant IL-22 (rIL-22), the suppressed proliferation of HaCaT by UVB was rescued. In addition, we found that the production of UVB-induced pro-inflammatory cytokines, such as IL-1α, IL-6 and IL-18, was increased by the treatment of rIL-22. Taken together, IL-22 plays a critical role in inflammation by UVB irradiation. And it suggests that UVB-induced skin inflammation could effectively be controlled by the regulation of IL-22 production and its action on keratinocytes. Note: This abstract was not presented at the meeting. Citation Format: Yejin Kim, Hyemin Kim, Jiwon Choi, Mirim Jang, Jiyea Choi, Jae Seung Kang, Wang Jae Lee. The role of Interleukin (IL)-22 on the UVB-induced proliferation and inflammation of human keratinocyte cell line, HaCaT. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4900. doi:10.1158/1538-7445.AM2014-4900