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Updated: Sep 18, 2026

Activation and Measurement of NLRP3 Inflammasome Activity Using IL-1β in Human Monocyte-derived Dendritic Cells
Published on: May 22, 2014
EGR1 coordinates a nuclear IL-33-phosphorylated STAT3 transcriptional complex to promote IL31 expression in
Euitaek Jung1, Yena Choi1, Junekyu Han1
1Department of Biological Sciences, College of Life Sciences, Konkuk University, Seoul, 05029, Republic of Korea.
Abstract:
Interleukin (IL)-31 is a pruritogenic cytokine implicated in atopic dermatitis (AD), but its transcriptional regulation in epidermal keratinocytes remains unclear. We investigated whether early growth response 1 (EGR1) links Toll-like receptor (TLR)1/2 signaling to IL31 expression through nuclear IL-33 and signal transducer and activator of transcription 3 (STAT3). EGR1 and IL-31 were prominent in human AD skin, and the TLR1/2 agonist Pam3CSK4 induced keratinocyte IL31 expression, EGR1 accumulation, and STAT3 phosphorylation. DNA affinity precipitation showed recruitment of EGR1, phosphorylated STAT3 (p-STAT3), and IL-33 to proximal IL31 promoter elements, while interaction and proximity-labeling analyses supported an EGR1-associated complex containing IL-33 and p-STAT3. Depletion of EGR1, IL-33, or STAT3 disrupted coordinated promoter recruitment. The EGR1 inhibitor IT25 impaired EGR1 promoter binding, suppressed Pam3CSK4-induced IL31 expression, and reduced epidermal IL-31 in house dust mite-exposed mouse skin. These findings identify EGR1 as a TLR1/2-responsive transcriptional organizer coordinating nuclear IL-33 and activated STAT3 at the IL31 promoter and linking innate receptor activation to keratinocyte IL31 expression.
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