ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2026
Single-cell transcriptomic analysis identifies a MIF-driven keratinocyte-macrophage-Th2 axis as a key inflammatory circuit in atopic dermatitis.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 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
backgroundAtopic dermatitis (AD) is a chronic inflammatory skin disorder involving complex interactions among multiple cell types. The cellular heterogeneity and intercellular communication networks driving AD pathogenesis remain to be fully elucidated.
methodsSingle-cell RNA sequencing datasets were employed to identify cell types in lesional skin of AD patients and analyze the transcriptomic characteristics of keratinocytes, T cells, and macrophages. Cell clusters were identified based on marker gene expression, and intercellular communication networks were analyzed to investigate cell-cell interactions. The findings were validated using in vitro cell models (HaCaT, HEK, primary keratinocytes, and THP-1 cells) and an MC903-induced AD mouse model, with MIF expression assessed by qPCR and Luminex. Immunofluorescence staining was used to evaluate the distribution and aggregation of macrophages. Functional studies were conducted using MIF098 to inhibit MIF signaling.
resultsscRNA-seq revealed significant cellular remodeling in AD lesions, with marked enrichment of keratinocytes, T cells, and macrophages. The proportion of Th2 cells was increased in AD lesion tissues, and an MRC1
conclusionOur findings identify a critical role for the MIF signaling axis in mediating crosstalk between proliferative keratinocytes and M2-polarized macrophages, thereby promoting Th2-driven inflammation in AD. Targeting MIF may represent a potential therapeutic strategy for AD.
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