Role of the STAT3 Signaling Pathway in Cell Proliferation and Inflammation in Psoriasis and Approaches for Targeted Therapies: A Review

22 April 2026 : Review article

Limin Li^{CE 1}, Lu Chen^{B 1}, Cai Zhang^{BEF 2}, Wenchao Yao^{D 1}, Zhengxiao Li^{G 3}, Faming Tian^{G 1,2*}

DOI: 10.12659/MSM.952449

Med Sci Monit 2026; 32:e952449

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Introduction Molecular Mechanism of the STAT3-Signaling Pathway Future Directions Conclusions References

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Table 2 Summary of the mechanisms of STAT3 in psoriasis pathogenesis.

Cell type	Mechanism of STAT3 action	Impact on psoriasis	References
Keratinocytes	Promotes proliferation, inhibits apoptosis, upregulates K16/K17, down-regulates differentiation markers such as filaggrin	Epidermal hyperplasia, barrier dysfunction, release of inflammatory factors (eg, IL-6, CXCL1)	[,–]⁴⁸
Th17 cells	Promotes Th17 differentiation, enhances IL-17 expression, synergizes with RORγt/AHR	Amplifies inflammation, establishes a positive feedback loop in the IL-17/IL-23 axis	[–]³⁰
DCs	Enhances antigen-presenting capacity, promotes IL-23 secretion, recruits neutrophils	Activates Th17 cells, sustains chronic inflammation	[–]³⁵
Macrophages	Promotes M1 polarization (pro-inflammatory), inhibits M2 polarization (anti-inflammatory), regulates metabolic reprogramming (eg, glycolysis)	Increases release of inflammatory factors (TNF-α, IL-6), forms a positive feedback loop with NF-κB	[–]³⁸
Neutrophils	Regulates CXCL1/CXCL2/CXCL8 expression, induces NETs formation, activates the TLR9-IL-17 pathway	Enhances inflammatory cell infiltration, causes tissue damage, sustains inflammation	[–]⁴⁸
NETs – neutrophil extracellular traps; DCs – dendritic cells.

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