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. Author manuscript; available in PMC: 2009 Oct 1.
Published in final edited form as: Br J Dermatol. 2008 Aug 5;159(5):1092–1102. doi: 10.1111/j.1365-2133.2008.08769.x

Fig 7.

Fig 7

Working model of the likely contributions of the Th17 cytokines interleukin (IL)-17 and IL-22, and the Th1 cytokine interferon (IFN)-γ, to psoriasis. Th1, T helper 1 cells; Th17, T helper 17 cells; KC, keratinocyte; Neut, neutrophil; DC, dendritic cell. Th17 cells produce IL-17 that induces KCs to produce ELR+ chemokines and CCL20 bringing neutrophils, DCs and T cells into the psoriatic lesion. IL-22, produced by Th17 cells and other T cells, downregulates KC differentiation genes. IL-17 and IL-22 both upregulate S100A7 (psoriasin). Th1 cells release IFN-γ, inducing keratinocytes to produce CXCL9, CXCL10 and CXCL11 that cause influx of CXCR3-bearing T cells into the lesion.

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