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.
Keywords: Keratinocytes; Psoriasis; SERPINB3/4; T cells; TEAD4.
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