Study Identifies Histone H4K12 Lactylation as Key Regulator in IL-17 Signaling Pathway of Psoriasis

A recent study published in *Nature Communications* has identified a new epigenetic mechanism that contributes to the progression of psoriasis, a chronic inflammatory skin condition. Researchers have found that histone lactylation at lysine 12 on histone H4 (H4K12la) in keratinocytes plays a key role in regulating an interleukin-17 (IL-17)-dependent signaling pathway. This discovery highlights an unrecognized aspect of inflammatory signaling within the skin and provides new insights into the molecular processes underlying psoriasis.

The study focuses on keratinocyte-specific modifications, particularly H4K12 lactylation, which appears to drive a non-canonical IL-17-dependent pathway involved in psoriasis development. Histone lactylation is an epigenetic modification where lactate molecules attach to histones, influencing gene expression. The findings suggest that this specific modification may act as a critical regulator of inflammation in psoriatic skin. Researchers believe this mechanism could help explain how certain inflammatory signals are amplified during disease progression, offering potential avenues for further investigation into therapeutic strategies targeting these pathways.

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Date: September 30, 2025

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Author

Mark Chiang