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. 2015 Nov 6;28(4):181–188. doi: 10.1093/intimm/dxv063

Fig. 1.

Fig. 1.

The inflammatory circuit of TNFα, IL-6, IL-23 and IL-17 in the pathogenesis of psoriasis. The persistent production of TNFα and other inflammatory cytokines activates DCs to produce IL-23, and IL-6, together with TGFβ, induces naive CD4+ T cells to differentiate into IL-17-producing T cells. IL-23 directly activates macrophages (Mϕ) to produce inflammatory cytokines such as TNFα and IL-1; IL-23 also promotes Th17 cell differentiation into highly pathogenic Th17 cells and activates γδ T cells, both cell types constantly produce IL-17A, IL-17F, IL-6 and TNFα. IL-17 activates epithelial cells (e.g. keratinocytes) and endothelial cells to produce a variety of inflammatory cytokines, chemokines and AMPs. The inflammatory cytokines induced by IL-17 promote the expansion of IL-17-producing γδ T or Th17 cells whereas the chemokines recruit more neutrophils or IL-17-producing T cells to sites of inflammation in the skin, which produces a positive feed-forward mechanism and further amplifies local inflammatory responses to incite cytokine storms in psoriasis.