ArticleJCI insight2025
DGAT2 reduction and lipid dysregulation drive psoriasis development in keratinocyte-specific SPRY1-deficient mice.
Article in JCI insight, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Transcriptome and proteome combined analysis of wool fiber diameter regulation mechanism.Animal bioscience · 2026Article
- Causal Effects of Diet on Atopic Dermatitis: A Mendelian Randomization Study Implicating Lipid Pathways and Clinical Implications.Clinical, cosmetic and investigational dermatology · 2026Article
- Licoisoflavone B alleviates psoriasis via SCD1-targeted lipid metabolism reprogramming and suppression of Th17/IL-17-mediated inflammation.Frontiers in pharmacology · 2026Article
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
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Authors and funding
9 authors.
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Abstract
Psoriasis is a chronic autoimmune skin disease characterized by abnormal keratinocyte proliferation and immune dysregulation. Altered lipid metabolism has been implicated in its pathogenesis, but the underlying mechanisms remain unclear. In this study, we generated a keratinocyte-specific Sprouty RTK signaling antagonist 1 (SPRY1) knockout (Spry1ΔEpi) mouse model, which exhibits psoriasis-like symptoms. Using both psoriasis patient samples and Spry1ΔEpi mice, we investigated the role of diacylglycerol acyltransferase 2 (DGAT2) in psoriasis. Our results show that DGAT2 expression was reduced and glyceride metabolism was disrupted in psoriatic lesions in both patients with psoriasis and Spry1ΔEpi mice. Lipidomic analysis revealed significant alterations in glycerides, glycerophospholipids, sphingolipids, and fatty acids in Spry1ΔEpi mice. At the cellular level, DGAT2 downregulation and lipid dysregulation enhanced TLR3-mediated inflammatory signaling in keratinocytes. Furthermore, increased DGAT2 secretion from keratinocytes promoted CD8+ T cell activation, proliferation, and survival, amplifying psoriatic inflammation. These findings highlight the role of DGAT2 and lipid metabolism in the pathogenesis of psoriasis and reveal their interaction with immune responses in psoriasis.
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