ArticleiScience2026
Interleukin 4-driven loss of stromal LIF signaling affects immune responses and cell-cell adhesion in atopic dermatitis.
Article in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Atopic dermatitis (AD) involves immune dysregulation, epidermal barrier defects, and impaired cell-cell adhesion, yet the contribution of dermal fibroblasts (FBs) remains poorly understood. Here we show that leukemia inhibitory factor (LIF), a cytokine produced by dermal FBs, is downregulated in AD skin-driven by the Th2 cytokine IL-4-and that this loss triggers a self-amplifying inflammatory circuit. Using single-cell RNA sequencing, immunofluorescence, keratinocyte (KCs)-FBs co-cultures, and functional adhesion assays, we demonstrate that reduced LIF signaling elevates IL-6 production in KCs, activates ERK1/2, and decreases membrane expression of the desmosomal protein desmoglein 1 (DSG1), impairing epidermal cohesion. DSG1 loss further amplifies IL-6 secretion, perpetuating the cycle. Blocking IL-6 or ERK1/2 signaling rescues adhesion defects. These findings identify a stromal-epidermal axis linking Th2 inflammation to barrier dysfunction and offer mechanistic insights into AD chronicity.
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