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. 2021 Jul 21;10(15):3199. doi: 10.3390/jcm10153199

Figure 1.

Figure 1

Summarized molecular mechanism of psoriasis. IFN-α released from activated pDCs stimulates myeloid DCs to produce TNF and IL-23. TNF activates DCs in an autocrine manner and enhances the inflammatory responses of various immunocytes. Naïve CD4-positive T cells differentiate into Th17 cells in the presence of the transforming growth factor (TGF)-β, IL-21, and IL-6. The pathogenicity of Th17 cells is potentiated by IL-23. IL-17 and IL-22 are produced by Th17 and other cells with more innate characteristics (e.g., innate lymphoid cell (ILC)-3 and gamma delta T cells). IL-17 and Il-22 induce epidermal hyperproliferation. IL-17 and TNF synergistically accelerate the production of inflammatory cytokines and chemokines from the epidermal keratinocytes, resulting in a vicious circle of inflammatory reactions.