Figure 1.

Tumor necrosis factor(TNF-α)/interleukin-23 (IL-23)/IL-17 axis in the pathogenesis of psoriasis. Dendritic cells activated by various stimuli in the lesional skin secrete TNF-α which acts on themselves in an autocrine manner and induces IL-23 secretion. The IL-23 promotes the proliferation and survival of Th17 cells. The activated Th17 cells overproduce IL-17A or IL-22 which act on keratinocytes and induce their proliferation and production of TNF-α, antimicrobial peptides, or chemokines C-X-C motif ligand 1 (CXCL1)/8, C-C-motif ligand 20 (CCL20), which further recruit neutrophils, lymphocytes, or monocytes. The activation of keratinocytes by IL-17A or TNF-α induces the expression of keratins 6 and 16, which are associated with acanthosis and reduced turnover time in the epidermis.