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 its receptor 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 of UVB-irradiated human keratinocytes, HaCaT. First, we found the increase of IL-22 mRNA expression was increased in HaCaT by UVB irradiation (150J/m2). When UVB-irradiated HaCaT was cultured in the presence of recombinant IL-22, the suppressed proliferation of HaCaT by UVB was rescued. It was closely related with the progression of cell cycle in UVB-irradiated HaCaT. We confirmed that the hyperproliferation and cell cycle progression of UVB-irradiated HaCaT by the addition of activated T cells or its culture supernatant. Taken together, IL-22 plays a critical role in the deterioration of epidermal hyperplasia 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.
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