Figure 4 STAT3 regulates neutrophil recruitment and NETosis in psoriasisSTAT3 regulates the recruitment and activation of neutrophils in psoriasis. It promotes skin infiltration by facilitating the release of chemokines by neutrophils. Activated neutrophils cause tissue damage through reactive oxygen species (ROS) and proteases, while STAT3-triggered neutrophil extracellular trap cell death (NETosis) amplifies the inflammatory response through the Toll-like receptor 9 (TLR9)/IL-17 axis and promotes the progression of psoriasis. IL-17 activates JAK2/STAT3 in keratinocytes to drive neutrophil chemotaxis. In the pathological microenvironment of psoriasis, IL-17 can specifically act on skin keratinocytes, inducing the activation of the intracellular JAK2/STAT3 signaling pathway. After this pathway is activated, it further upregulates the transcription and secretion of chemokines such as C-X-C motif chemokine ligand 1 (CXCL1), CXCL2, and CXCL8, recruiting neutrophils to gather at the skin inflammatory site through chemotaxis. This amplifies the local inflammatory cascade reaction, thereby promoting the occurrence and pathological progression of psoriasis. (Created with BioRender.com).