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PU.1 drives psoriasis pathogenesis by promoting intermediate monocytes-to-M1 macrophage differentiation through Dectin-1 signaling
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DOI:10.1016/j.jaut.2026.103610.png)
Abstract
En 中文
• Single-cell RNA-seq detects expanded intermediate monocytes (IMs) in psoriasis patients with high differentiationcapacity. • Transcription factor PU.1 governs pathogenic differentiation of IMs into pro-inflammatory M1 macrophages in psoriatic lesions. • PU.1 transcriptionally activates Dectin-1 to initiate SYK/NF-κB signaling and drive IM-to-M1 polarization. • Pharmacological inhibition of PU.1 with the BET inhibitor NHWD-870 attenuates psoriasiform inflammation in vivo.
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