Fig. 9: Schematic diagram of MiR-193b-3p/ERBB4 axis involved in the pathogenesis of psoriasis. | Cell Death & Disease

Fig. 9: Schematic diagram of MiR-193b-3p/ERBB4 axis involved in the pathogenesis of psoriasis.

From: MiR-193b-3p–ERBB4 axis regulates psoriasis pathogenesis via modulating cellular proliferation and inflammatory-mediator production of keratinocytes

Fig. 9

When keratinocytes are in a psoriasis-related inflammatory environment (or are subjected to external stimuli), the expression of miR-193b-3p is downregulated, while that of ERBB4 is upregulated. ERBB4 promotes the proliferation and expression of inflammatory genes (IL-6, CXCL1, CCL20, BD-2, etc.) in keratinocytes, leading to the activation of keratinocytes and resulting in the recruitment and activation of relevant immune cells (including Th1, Th17, Th22, etc.). The activated immune cells secrete pro-inflammatory mediators (TNF-α, IL-17, IL-22, etc.), which further cause the downregulation of miR-193b-3p (ERBB4 is upregulated) in keratinocytes, forming a feedback loop and leading to the expansion of the inflammatory response in psoriasis.

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