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Targeting the Plasticity of Psoriasis

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Presentation on theme: "Targeting the Plasticity of Psoriasis"— Presentation transcript:

1 Targeting the Plasticity of Psoriasis
Jack L. Arbiser, Justin Elsey  Journal of Investigative Dermatology  Volume 138, Issue 4, Pages (April 2018) DOI: /j.jid Copyright © 2017 The Authors Terms and Conditions

2 Figure 1 Known signaling abnormalities in psoriasis. Every layer of the skin is affected, with loss of AP-1 and activation of NF-κB giving rise to hyperkeratosis in the stratum corneum. NF-κB activates the calprotectin complex S100A8/A9, which can chelate zinc, which has both anti-infective and proinflammatory activity. The lower layers of the epidermis have decreased ceramide levels, due to either insufficient production of ceramides or rapid metabolism to sphingosine-1 phosphate, which promotes proliferation and inflammation. These effects of ceramide deficiency may be mediated in part by IL-22. In the basal layer of the skin, Rac activation promotes keratinocyte production of cytokines, such as IL-21, vascular endothelial growth factor, angiopoietin-2, IL-17, and TNF-α, which attract and maintain lymphocytes in the upper dermis. Th, T helper. Journal of Investigative Dermatology  , DOI: ( /j.jid ) Copyright © 2017 The Authors Terms and Conditions


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