The pathophysiology of psoriasis
The past 25 years of research and clinical practice have revolutionized our understanding of the pathogenesis of psoriasis as the dysregulation of immunity triggered by environmental and genetic stimuli. Psoriasis was originally regarded as a primary disorder of epidermal hyperproliferation. However, experimental models and clinical results from immunomodulating therapies have refined this perspective in conceptualizing psoriasis as a genetically programmed pathologic interaction between resident skin cells, infiltrating immunocytes and a host of proinflammatory cytokines, chemokines and growth factors produced by these immunocytes. Two populations of immunocytes and their respective signaling molecules collaborate in the pathogenesis: innate immunocytes, mediated by antigen presenting cells (including natural killer T lymphocytes, Langerhans cells and neutrophils) and acquired or adaptive immunocytes, mediated by mature CD4+ and CD8+ T lymphocytes in the skin. Such dysregulation of immunity and subsequent inflammation is responsible for the development and perpetuation of the clinical plaques and histological inflammatory infiltrate characteristic of psoriasis.
KeywordsNatural Killer Psoriatic Skin Immunologic Synapse Psoriatic Lesion Chronic Plaque Psoriasis
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