Keratin 6A (KRT6A) is involved in the pathogenesis of various skin diseases. However, the reports on the roles of KRT6A in atopic dermatitis (AD) are limited. This study aimed to investigate the potentials of KRT6A in AD. mRNA levels were detected by RT-PCR. Cytokine release was determined by ELISA. Protein expression was determined using Western blot. Cell viability was determined by CCK-8. Cytotoxicity was detected by LDH assay. Cell death was determined by TUNEL. The pyroptosis of keratinocytes was detected using flow cytometry. We found that KRT6A was overexpressed in AD patients. Moreover, KRT6A was stimulated after exposed to proinflammatory cytokines. Overexpressed KRT6A suppressed inflammatory response, while KRT6A knockdown exerted the opposite effects. Overexpressed KRT6A suppressed inflammation-induced pyroptosis of keratinocytes. Additionally, KRT6A negatively regulated interleukin-17a (IL-17a) expression, blocking IL-17 signaling. IL-17a overexpression antagonized the effects of KRT6A and promoted pyroptosis of keratinocytes. In conclusion, KRT6A exerted protective functions in AD via regulating IL-17 signaling. This KRT6A/IL-17 may be a novel target for AD.

中文翻译：

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KRT6A 通过阻断 IL-17 信号传导抑制 IL-1β 介导的角质细胞焦亡

角蛋白6A（KRT6A）参与多种皮肤病的发病机制。然而，关于 KRT6A 在特应性皮炎 (AD) 中的作用的报道有限。本研究旨在探讨 KRT6A 在 AD 中的潜力。通过RT-PCR检测mRNA水平。通过ELISA测定细胞因子释放。使用蛋白质印迹测定蛋白质表达。通过CCK-8测定细胞活力。通过LDH测定检测细胞毒性。通过TUNEL测定细胞死亡。使用流式细胞术检测角质形成细胞的焦亡。我们发现 KRT6A 在 AD 患者中过度表达。此外，KRT6A 在暴露于促炎细胞因子后受到刺激。过度表达 KRT6A 会抑制炎症反应，而 KRT6A 敲低则会产生相反的效果。过表达的 KRT6A 抑制炎症诱导的角质形成细胞焦亡。此外，KRT6A 负向调节白细胞介素 17a (IL-17a) 表达，阻断 IL-17 信号传导。IL-17a过表达拮抗KRT6A的作用并促进角质形成细胞焦亡。总之，KRT6A 通过调节 IL-17 信号传导在 AD 中发挥保护功能。KRT6A/IL-17 可能是 AD 的新靶标。