IL-22 is known to mediate inflammation in psoriasis, while IL-22 binding protein (IL-22BP) binds IL-22 to suppress IL-22 signaling. However, the function of IL-22 in regulating apoptosis in psoriasis remains poorly understood. In this study, we found that IL-22/IL-22R1 in lesional skin and IL-22 in serum from psoriatic patients were highly upregulated compared with healthy controls, while IL-22BP was not changed. Correlations between IL-22/IL-22R1 levels and the thickness of psoriatic lesions suggested that IL-22 might positively regulate abnormal hyperplasia in psoriasis. Apoptotic keratinocytes were increased only in stratum corneum, but not in spinous and basal layers of psoriasis. Moreover, IL-22 promoted cell viability in human epidermal keratinocytes (HEKs). The apoptosis induced by TNF-α and IFN-γ was inhibited in HEKs treated with IL-22, since that IL-22 upregulated Bcl-xL and downregulated Bax production in HEKs in the presence of TNF-α and IFN-γ. In addition, IL-22BP could counteract the anti-apoptotic effect of IL-22. Our finding demonstrates that IL-22 might play an anti-apoptosis role on keratinocytes to balance cell proliferation and apoptosis in psoriatic epidermis.

已知 IL-22 介导银屑病炎症，而 IL-22 结合蛋白 (IL-22BP) 结合 IL-22 以抑制 IL-22 信号传导。然而，IL-22 在银屑病中调节细胞凋亡的功能仍知之甚少。在这项研究中，我们发现与健康对照相比，银屑病患者皮损皮肤中的IL-22/IL-22R1和血清中的IL-22高度上调，而IL-22BP没有变化。 IL-22/IL-22R1水平与银屑病皮损厚度之间的相关性表明IL-22可能正向调节银屑病的异常增生。凋亡的角质形成细胞仅在角质层中增加，而在牛皮癣的棘层和基底层中不增加。此外，IL-22 还能促进人表皮角质形成细胞 (HEK) 的细胞活力。在用 IL-22 处理的 HEK 中，TNF-α 和 IFN-γ 诱导的细胞凋亡受到抑制，因为在 TNF-α 和 IFN-γ 存在的情况下，IL-22 上调 HEK 中的 Bcl-xL 并下调 Bax 的产生。此外，IL-22BP可以抵消IL-22的抗凋亡作用。我们的研究结果表明，IL-22 可能对角质形成细胞发挥抗凋亡作用，以平衡银屑病表皮中的细胞增殖和凋亡。