Figure 1.

Current model of psoriasis immunopathology ³⁰ , ⁹³ , ⁹⁴ (1) Activation of plasmacytoid dendritic cells (pDCs) and interleukin (IL)‐23‐producing epidermal DCs due to keratinocyte damage. (2) T helper (Th)17 cell polarization and clonal expansion is triggered. T‐cell activation leads to production of proinflammatory cytokines. IL‐23 promotes Th17 cell clonal expansion and differentiation. (3) IL‐17 +/– tumour necrosis factor alpha (TNF‐α) induces further inflammation with terminal keratinocyte differentiation and proliferation – forming a psoriatic plaque. (4) A feedforward inflammatory response is induced, with IL‐17 inducing psoriasis‐related gene expression in keratinocytes, driving further inflammation. eDCs, epidermal DCs; IFN, interferon; LC, Langerhans cell; LL‐37, cathelicidin antimicrobial peptide; TRM, tissue‐resident memory cell. [Colour figure can be viewed at wileyonlinelibrary.com]