The effect of interleukin (IL)-22 on human keratinocyte cell line irradiated by UVB

Abstract

Interleukin (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. It has recently been reported that IL-22 plays a critical role in the maintenance of epidermal homeostasis by controlling cell cycle of keratinocytes. In addition, it is already known that ultraviolet B (UVB) radiation induces skin inflammation. However, there are no reports regarding the role of UVB on the production of IL-22 and its receptor expression. Therefore, I investigated the role of IL-22 on the proliferation of UVB-irradiated human keratinocyte cell line, HaCaT and the induction of skin inflammation in terms of IL-22Rα expression on HaCaT. The expression of IL-22Rα mRNA and its protein in HaCaT was increased by UVB (100 J/m2) irradiation. Interestingly, the translocation of IL-22Rα from cytosol to membrane was increased by UVB irradiation. It is generally known that UVB suppresses the proliferation of HaCaT, but the suppressed proliferation of UVB-irradiated HaCaT was recovered by the treatment of recombinant IL-22 and culture supernatant of activated PBMCs. Finally, the production of pro-inflammatory cytokines, such as IL-1α, IL-6 and IL-18, was increased from UVB-irradiated HaCaT by the treatment of rIL-22. Taken together, IL-22 increases skin inflammation and the proliferation of HaCaT through the interaction with up-regulated IL-22Rα on HaCaT by UVB irradiation.