●Psoriasis is a complex immune-mediated disorder that presents as inflammatory plaques in the skin. Dysregulation or alteration of components of the innate and adaptive immune systems, keratinocyte function, and vascular structure contribute to the manifestations of this disease.
●Plasmacytoid and myeloid dendritic cells are key contributors to development of inflammation in psoriasis. Interferon (IFN)-alpha produced by plasmacytoid dendritic cells stimulates the activation of myeloid dendritic cells, which contribute to the adaptive immune response through the activation of T cells.
●Interleukin (IL) 23 and IL-12 produced by activated macrophages and myeloid dendritic cells promote the development of T helper type 17 (Th17)/Tc17 and T helper type 1 (Th1) cells, respectively. Th17 and Tc17 cells play a major role in the pathogenesis of psoriasis.
●Keratinocytes may contribute to the initiation of psoriasis via the production of antimicrobial peptides. Epidermal hyperplasia is driven by cytokines that stimulate keratinocyte activation and proliferation.
●Knowledge of the pathophysiology of psoriasis is evolving. Advances in the understanding of the mechanisms of disease will likely contribute to the development of new therapeutic agents and improved patient outcomes.
