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. Author manuscript; available in PMC: 2020 Nov 1.
Published in final edited form as: J Invest Dermatol. 2019 Nov;139(11):e133–e142. doi: 10.1016/j.jid.2019.08.437

Figure 1. Simplified overview of interrelation between psoriasis predisposing factors, inflammatory mechanisms, clinical manifestations, and consequences.

Figure 1.

Crosstalk between the innate and adaptive immune systems involves secretion of IL-12 and IL-23, which are important for priming and maintaining Th1 and Th17 responses. Inflammatory responses prime keratinocytes that in turn amplify the inflammatory response and “feed forward,” creating a sustaining cycle of inflammation. These inflammatory responses shape the clinical manifestations of psoriasis, which exist between pustular forms (dominated by higher IL-36 responses) and plaque psoriasis (characterized by high IL-17A).