ArticleFrontiers in immunology2026
Plasmacytoid dendritic cells alleviate atopic dermatitis by suppressing Th2 inflammation via the IFN-α/IFNAR1 pathway.
Article in Frontiers in immunology, 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
Background and objective: Atopic dermatitis (AD) is a chronic immune-mediated inflammatory skin disease characterized by persistent pruritus and eczematous lesions. Its core pathophysiology involves Th2-skewed immune responses and epidermal barrier dysfunction. Plasmacytoid dendritic cells (pDCs), known for their potent production of type I interferons, have demonstrated immunomodulatory roles in various diseases, including allergic asthma. However, their specific function and underlying mechanisms in AD remain poorly defined. This study aims to investigate the role of pDCs in AD and elucidate their molecular regulatory pathways. Methods: We employed an integrative approach combining transcriptomic analysis, flow cytometry, an MC903-induced murine model of AD, Results: pDCs were significantly elevated in the peripheral blood of AD patients and were associated with increased expression of Th2 cytokines. In the MC903-induced murine model, pDCs showed dynamic accumulation in skin lesions and draining lymph nodes. Expansion of pDCs by FLT3L markedly alleviated AD-like skin inflammation, suppressed Th2 cytokines (IL-4, IL-13) and IgE production, and enhanced the expression of epidermal barrier proteins. In contrast, depletion of pDCs by 120G8 exacerbated the inflammatory phenotype. Importantly, the anti-inflammatory effects of pDCs were abolished in IFNAR1-deficient mice, indicating that pDCs exert their immunosuppressive function in AD primarily through the IFN-α/IFNAR signaling axis. Conclusion: This study is the first to systematically demonstrate the immunosuppressive role of pDCs in AD. We show that pDCs negatively regulate Th2 inflammation and maintain barrier integrity via the IFN-α/IFNAR1 pathway. These findings provide a theoretical and experimental foundation for targeting pDCs and their downstream signaling as a novel therapeutic strategy in AD.
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