Keratin 17 (K17) is a multifaceted cytoskeletal protein that is not commonly expressed in the epidermis under normal physiological conditions. However, in psoriasis, K17 is overexpressed in the suprabasal layer of the epidermis and plays an important role in the pathogenesis of the disease. In this review, we have summarized our findings and those reported in other studies concerning the pathogenic functions of K17, as well as the mechanisms underlying the increase in K17 expression in psoriasis. K17 exerts both pro-proliferative and pro-inflammatory effects on keratinocytes. Moreover, K17 peptides trigger autoreactive T cells and promote psoriasis-related cytokine production. In turn, these cytokines modulate the expression, stability, and protein–protein interactions of K17 through transcriptional and translational regulation and post-translational modification of K17 in keratinocytes. Thus, a K17/T-cell/cytokine autoimmune loop is implicated in the pathogenesis of psoriasis, which is supported by the fact that therapies targeting K17 have achieved good outcomes in psoriasis-like mouse models. Future perspectives of K17 in psoriasis have also been discussed to provide potential directions for further studies.

角蛋白 17 (K17) 是一种多方面的细胞骨架蛋白，在正常生理条件下通常不会在表皮中表达。然而，在银屑病中，K17 在表皮基底层过度表达，在疾病的发病机制中起重要作用。在这篇综述中，我们总结了我们的研究结果和其他研究中报道的关于 K17 致病功能的研究结果，以及 K17 在银屑病中表达增加的机制。K17 对角质形成细胞具有促增殖和促炎作用。此外，K17 肽触发自身反应性 T 细胞并促进银屑病相关细胞因子的产生。反过来，这些细胞因子调节表达、稳定性、通过角质形成细胞中 K17 的转录和翻译调控以及翻译后修饰，K17 和蛋白质-蛋白质相互作用。因此，K17/T 细胞/细胞因子自身免疫环与银屑病的发病机制有关，这得到了靶向 K17 的疗法在银屑病样小鼠模型中取得良好结果的支持。还讨论了 K17 在银屑病中的未来前景，为进一步研究提供潜在方向。