Fig. 1

T cell transcriptional regulation mechanism in psoriasis. Psoriasis is driven by many nonspecific triggers. Triggers such as infections and physical injury stimulate DCs to release pro-inflammatory factors (IL-6, IL-1β, IL-21, IL-23, TNF-α and IL-12). These cytokines stimulate the activation of naive CD4 + T cells and secrete IL-12, IL-23 and IL-6, IL-10 and TGF-β, IL-4 differentiated into Th1 cells, Th17 cells, Treg cells and Th2 cells, respectively. IL-12 combines with naive CD4 + T cell surface receptor, IL-12R, and their interaction leads to activation of the transcription factors STAT1 and T-bet, thereby promoting the polarization of Th1 cells. T-bet and STAT1 form a positive feedback regulatory loop for upregulating IL-12 and promoting Th1 polarization. Th17 cells are differentiated by ROR-γt regulation is also regulated by JAK–STAT3 pathway. IL-6 produced in response to inflammation continuously activates the STAT3 pathway, which in turn induces IL-21 expression and forms an IL-21/STAT3 autocrine loop, thereby causing sustained activation of STAT3, upregulation of ROR-γt for Th17 differentiation. The differentiation of Th2 cells is regulated by GATA 3. The balance of Th1, Th17 and Th2 is an important factor affecting the development of psoriasis. Treg cells can suppress the activities of other immune effector cells, such as Th1 and Th17 cells, through either direct contact or the secretion of suppressive cytokines, such as IL-10 and transforming growth factor (TGF)-β. This figure was created with Figdraw.com