ArticleJID innovations : skin science from molecules to population health2026
Characterizing Keratinocyte-Derived Extracellular Vesicles in UVB-Irradiated Murine Skin.
Article in JID innovations : skin science from molecules to population health, 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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6 authors.
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Abstract
UVB radiation is a potent trigger for photosensitive autoimmune diseases, yet the mechanism through which UVB-induced superficial epidermal damage drives deeper systemic inflammation remains poorly understood. Extracellular vesicles (EVs) have emerged as key mediators of UVB-induced immune activation and have also been specifically implicated in the pathogenesis of multiple photosensitive autoimmune diseases, therefore suggesting the possibility that UVB-induced EVs could be involved in driving this systemic inflammation. In this study, C57BL/6 mice were exposed to repeated dorsal UVB irradiation, and dermal tissue was processed to isolate EVs through sequential ultracentrifugation and density-gradient purification. Transmission electron microscopy, ExoView, immunogold labeling, and western blotting confirmed the presence of EVs within the dermis, including those expressing cytokeratin 10, a keratinocyte differentiation marker. UVB-irradiated dermal EVs showed significantly higher cytokeratin 10 expression than sham controls, supporting their keratinocyte origin and demonstrating that EVs can traverse the epidermal-dermal junction. These findings provide direct evidence that UVB triggers the release of keratinocyte-derived EVs into the dermis, where they may serve as vehicles for inflammatory signaling and immune modulation. The identification of cytokeratin 10-positive EVs as mediators of epidermal-dermal crosstalk highlights a potential mechanism linking UVB exposure to systemic autoimmunity and suggests, to our knowledge, a previously unreported therapeutic targets to mitigate photodamage.
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