Multi-Modal Skin Atlas Identifies a Multicellular Immune-Stromal Community Associated with Disrupted Cornification and Specific T Cell Expansion in Atopic Dermatitis

    February 2026 in “ Nature Communications
    Evgenij Fiškin, Gökcen Eraslan, Maria B. Alora-Palli, Tanvi Jain, Juan Manuel Leyva-Castillo, Sean Kim, Heather Choe, Caleb A. Lareau, Helena Lau, Emily P. Finan, Isabella Teixeira-Soldano, Brenna LaBere, Anne Chu, Brian Woods, Janet Chou, Michal Slyper, Julia Waldman, Sabina A. Islam, Lynda C. Schneider, Wanda Phipatanakul, Craig Platt, Orit Rozenblatt-Rosen, Toni Delorey, Orr Ashenberg, Jacques Deguine, Gideon P. Smith, Raif S. Geha, Aviv Regev, Ramnik J. Xavier
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    TLDR A specific group of immune and skin cells may cause chronic inflammation in atopic dermatitis.
    The study presents a detailed multi-modal single-cell atlas of healthy and atopic dermatitis (AD) skin, analyzing 280,518 scRNA-seq profiles from 17 individuals, including 11 AD patients. It identifies 86 cell subsets, highlighting disrupted cornification in keratinocytes and a unique T cell state in AD skin characterized by IL13, IL22, and IL26 expression. This T cell state is clonally expanded and linked to type 2 and type 17 immune responses. The research reveals two multicellular immune-stromal communities in lesional AD skin, involving dendritic cells, T cells, and fibroblasts, which contribute to AD pathology through intercellular feedback loops. These findings underscore the complexity of AD and suggest potential therapeutic targets by understanding immune-stromal interactions and disrupted cornification processes.
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