Psoriasis vulgaris is a chronic inflammatory skin disease that results from the complex interplay between keratinocytes, dendritic cells, and T cells. Keratinocytes trigger innate and adaptive immune responses. Dermal myeloid dendritic cells regulate T cell activation and production of cytokines and chemokines that amplify inflammation. Most of the psoriatic T cells discretely produce interferon-γ, interleukin (IL)-17, and IL-22. The initiation phase of psoriasis involves Toll-like receptors, antimicrobial peptide LL37, and plasmacytoid dendritic cells. Keratinocytes are the main cutaneous cell type expressing IL-17 receptors and hence the immune circuit is amplified by keratinocytes upregulating mRNAs for a range of inflammatory products.
Key points
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Keratinocytes recruit inflammatory dendritic cells and IL-17–producing T cells through chemokine CCL20.
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Myeloid dendritic cells drive T-cell activation and psoriatic cytokine production through IL-23 and IL-12.
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IL-23 is required for T cells to produce IL-17. IL-23 is composed of two chains, the unique p19 chain and the p40 chain shared with IL-12.
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Distinct subsets of T cells produce interferon-γ, IL-17, and IL-22 in psoriatic lesions.
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Both αβ T cells and γδ T cells are increased in numbers and able to produce IL-17 in psoriatic skin.
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IL-17 is a key cytokine in psoriatic pathogenesis. Keratinocytes respond strongly to IL-17 but other cell types may also respond to IL-17 by activating inflammation-related genes.
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IL-17 can synergize with other cytokines, such as TNF and IL-22, for induction of key gene products related to the psoriasis phenotype.
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