Targeting the Plasticity of Psoriasis Jack L. Arbiser, Justin Elsey  Journal of Investigative Dermatology  Volume 138, Issue 4, Pages 734-736 (April 2018) DOI: 10.1016/j.jid.2017.11.030 Copyright © 2017 The Authors Terms and Conditions

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 2018 138, 734-736DOI: (10.1016/j.jid.2017.11.030) Copyright © 2017 The Authors Terms and Conditions