Psoriasis is a common chronic inflammatory disease with the prevalence rate of approximately 1–3 %. Currently, it is generally believed that the pathogenesis of psoriasis is a T-cell immune-mediated skin disease mediated by multiple genes and factors, and the interaction between keratinocytes and T cells. TEA domain family member 4 (TEAD4) is a transcription factor which regulates the expression of downstream genes in Hippo pathway and affects several biological processes, such as regulating cell differentiation and embryonic development. However, few studies have reported the role of TEAD4 in psoriasis and its possible regulatory mechanism. In this study, we found the expression level of TEAD4 in the skin of psoriasis was significantly higher than that of normal skin. In patients with the pathological keratinocytes, TEAD4 can transcriptionally regulate the expression of SERPINB3/4 and affect the secretion of chemokines, and the depletion of SERPINB3/4 inhibited the secretion of chemokines. In addition, the supernatant of keratinocytes of patients can significantly increase the migration ability of T cells, and the supernatant of T cells cultured by the supernatant of keratinocytes of patients can significantly enhance the proliferation ability of keratinocytes. Therefore, our results suggested that TEAD4 is a key regulatory factor in progression of psoriasis, and the crosstalk between keratinocytes and T cells mediated by TEAD4 plays a critical role in the psoriasis pathogenesis.

银屑病是一种常见的慢性炎症性疾病，患病率约为 1-3%。目前，普遍认为银屑病的发病机制是多基因和多因素介导的T细胞免疫介导的皮肤病，角质细胞与T细胞相互作用。TEA 域家族成员 4 (TEAD4) 是一种转录因子，可调节 Hippo 通路下游基因的表达并影响多种生物学过程，如调节细胞分化和胚胎发育。然而，很少有研究报道 TEAD4 在银屑病中的作用及其可能的调节机制。在本研究中，我们发现 TEAD4 在银屑病皮肤中的表达水平明显高于正常皮肤。在有病理性角质形成细胞的患者中，TEAD4可以转录调控SERPINB3/4的表达并影响趋化因子的分泌，SERPINB3/4的耗竭抑制了趋化因子的分泌。此外，患者角质细胞上清液可显着提高T细胞的迁移能力，患者角质细胞上清液培养的T细胞上清液可显着增强角质细胞增殖能力。因此，我们的结果表明 TEAD4 是银屑病进展的关键调控因子，并且由 TEAD4 介导的角质形成细胞和 T 细胞之间的串扰在银屑病发病机制中起关键作用。患者角质细胞上清液可显着提高T细胞的迁移能力，患者角质细胞上清液培养的T细胞上清液可显着增强角质细胞增殖能力。因此，我们的结果表明 TEAD4 是银屑病进展的关键调控因子，并且由 TEAD4 介导的角质形成细胞和 T 细胞之间的串扰在银屑病发病机制中起关键作用。患者角质细胞上清液可显着提高T细胞的迁移能力，患者角质细胞上清液培养的T细胞上清液可显着增强角质细胞增殖能力。因此，我们的结果表明 TEAD4 是银屑病进展的关键调控因子，并且由 TEAD4 介导的角质形成细胞和 T 细胞之间的串扰在银屑病发病机制中起关键作用。