ArticleIranian journal of basic medical sciences2026
STAT3 ablation in keratinocytes ameliorates allergic contact dermatitis in DNCB-induced mice model.
Article in Iranian journal of basic medical sciences, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Objectives: Allergic contact dermatitis (ACD) is a T cell-mediated type IV hypersensitivity reaction to haptens. Its pathogenesis involves keratinocyte dysfunction and dysregulation of the Signal Transducer and Activator of Transcription 3 (STAT3)-signaling pathway. However, the specific role of keratinocyte produced STAT3 in ACD remains unclear. To investigate the effect of keratinocyte (KC)-specific STAT3 conditional knockout on 1-Chloro-2,4-dinitrobenzene (DNCB)-induced ACD in mice. Materials and Methods: We generated keratinocyte-specific STAT3 conditional knockout (cKO) mice (K14-Cre⁺; STAT3 Results: Keratinocyte-specific STAT3 deletion significantly ameliorated ACD severity, evidenced by reduced TEWL values, enhanced epidermal barrier function, decreased dermatitis scores, reduced clinical dermatitis scores, decreased dermal inflammatory infiltration, lower spleen index, and attenuated mast cell degranulation. Molecular analysis revealed down-regulation of inflammation-related factors (IL-1β, IL-6, TNF-α, JAK2) and significant inhibition of STAT3 phosphorylation. Conclusion: Keratinocyte-specific STAT3 deletion alleviates epidermal barrier impairment and skin inflammation in ACD by inhibiting STAT3 phosphorylation and its downstream pro-inflammatory signaling.
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