Extracellular vesicles in atopic dermatitis: unraveling pathogenic mediators and engineering therapeutic vectors

25 May 20264 min read0 viewsJournal Feed

GIST (Key Takeaways)

Atopic dermatitis (AD) is a complex chronic inflammatory skin disease whose pathogenesis involves a vicious cycle of epidermal barrier defects, immune dysregulation, and microbial imbalance. Despite advances in targeted biologics and small−molecule drugs, there remains an unmet clinical need for safe, effective treatments that can simultaneously intervene in multiple pathological processes.
Extracellular vesicles (EVs), as key mediators of intercellular communication, play an increasingly prominent dual role in the pathophysiology and treatment of AD. This review systematically elaborates on this dialectical unity of EVs in AD.
In terms of pathological mechanisms, EVs derived from pathogens such as Staphylococcus aureus and Malassezia spp., as well as from host mast cells, act as active “nanoscale pathological messengers” that deeply participate in disease initiation and progression by delivering virulence factors, disrupting the skin barrier, driving Th2/Th17 immune polarization, and sustaining chronic inflammation.