ArticleImmunity2024
The transcription regulators ZNF750 and LSD1/KDM1A dampen inflammation on the skin's surface by silencing pattern recognition receptors.
Article in Immunity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- ZNF750 safeguards upper hair follicle homeostasis to prevent inflammatory skin disease.The Journal of investigative dermatology · 2026Article
- Review
- A tunable Cas12a platform for single-cell perturbation screening and CRISPRi.Nature communications · 2026Article
- HNRNPU and architectural lncRNAs as nuclear tethers of epithelial state stability.EMBO molecular medicine · 2026Review
- Squamous-state excursions activate APOBEC3A in cancer.bioRxiv : the preprint server for biology · 2026Article
- SPT6 maintains epidermal homeostasis by inhibiting an NF-κB-positive feedback loop to prevent excessive inflammation.Cellular & molecular immunology · 2026Article
- Inhibiting LSD1 unlocks retinoid AP-1 programming to activate epithelial immunity and skin tumor suppression.The Journal of clinical investigation · 2026Article
- ZNF750 suppresses esophageal squamous cell carcinoma by maintaining epithelial barrier-driven mucosal immune homeostasis.Biology direct · 2026Article
- Comparative analysis for optimal LSD1 inhibitors evaluation techniques: pros and cons.Journal of pharmaceutical analysis · 2026Review
- Nanozymes for ATP/cAMP balance restoration and ROS scavenging in inflammatory dermatosis treatment and recurrence prevention.Journal of nanobiotechnology · 2026Article
- ZNF750 Loss of Function Drives Spontaneous Psoriasiform Skin Inflammation.JID innovations : skin science from molecules to population health · 2026Article
- Transcriptional and epigenetic mechanisms governing epidermal stem cell regulation.Frontiers in cell and developmental biology · 2026Review
- Toll-like receptors in innate immunity and inflammation: from fundamental biology to clinic insights.Immunity & inflammation · 2026Review
- Hypoxia Induces Immunosuppression by Silencing STING in Cancer.Cancer research · 2025Article
- Targeting NLRP10 in Atopic Dermatitis: An Emerging Strategy to Modulate Epidermal Cell Death and Barrier Function.International journal of molecular sciences · 2025Review
- Keratinocyte-specific H4K12 lactylation drives a non-canonical IL-17-dependent signaling in psoriasis progression in mice.Nature communications · 2025Article
- The oesophagus as an immune organ.Nature reviews. Gastroenterology & hepatology · 2025Review
- C-terminal binding protein 2 interacts with JUNB to control macrophage inflammation.Life science alliance · 2025Article
- The antiprotease Spink7 promotes inflammation resolution by modulating multiple proteases activities during wound healing.Clinical and translational medicine · 2025Article
- Construction of a novel inflammatory-related prognostic signature of acute myelocytic leukemia based on conjoint analysis of single-cell and bulk RNA sequencing.Frontiers in immunology · 2025Article
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13 authors.
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Abstract
The surface of the skin is continually exposed to pro-inflammatory stimuli; however, it is unclear why it is not constantly inflamed due to this exposure. Here, we showed undifferentiated keratinocytes residing in the deep epidermis could trigger a strong inflammatory response due to their high expression of pattern recognition receptors (PRRs) that detect damage or pathogens. As keratinocytes differentiated, they migrated outward toward the surface of the skin and decreased their PRR expression, which led to dampened immune responses. ZNF750, a transcription factor expressed only in differentiated keratinocytes, recruited the histone demethylase KDM1A/LSD1 to silence genes coding for PRRs (TLR3, IFIH1/MDA5, and DDX58/RIG1). Loss of ZNF750 or KDM1A in human keratinocytes or mice resulted in sustained and excessive inflammation resembling psoriatic skin, which could be restored to homeostatic conditions upon silencing of TLR3. Our findings explain how the skin's surface prevents excessive inflammation through ZNF750- and KDM1A-mediated suppression of PRRs.
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