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JOURNAL ARTICLE
RESEARCH SUPPORT, N.I.H., EXTRAMURAL
RESEARCH SUPPORT, NON-U.S. GOV'T
REVIEW
The immunopathogenesis of psoriasis.
Dermatologic Clinics 2015 January
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.
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