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• W3044089550 abstract "T helper cells are crucial for psoriasis pathogenesis. Communication between T cells and psoriatic keratinocytes (KCs) helps drive the Th1 and Th17 response, but the underlying mechanism is not well-understood. Small extracellular vesicles (sEVs) are emerging mediators of intercellular communication. Here, we investigated the role of KC-derived sEVs in the Th1 and Th17 response in psoriasis. We isolated and characterized sEVs from KCs under normal (untreated) and psoriatic (cytokine-treated) conditions. sEVs under both conditions exhibited a cup-shaped morphology and expressed markers CD63 and CD81. sEVs from cytokine-treated KCs can be taken up by CD4+T cells, leading to the induction of Th1 and Th17 polarization. Small RNA sequencing revealed that miR-381-3p was significantly increased in sEVs from cytokine-treated KCs and in CD4+T cells from patients with psoriasis. Moreover, sEVs-containing miR-381-3p was responsible for sEVs-induced Th1 and Th17 polarization. We further found that the miR-381-3p targeted to the 3′ untranslated region of E3 ubiquitin-ligase UBR5 and stabilized RORγt protein expression. It also targeted to the 3′ untranslated region of FOXO1, associated with activated T-bet and RORγt transcription. Taken together, we propose that psoriatic KCs transfer miR-381-3p to CD4+T cells through sEVs, inducing Th1 and Th17 polarization and promoting psoriasis development. Our findings motivate future studies of KC-derived sEVs or their specific cargoes as therapeutic candidates for psoriasis. T helper cells are crucial for psoriasis pathogenesis. Communication between T cells and psoriatic keratinocytes (KCs) helps drive the Th1 and Th17 response, but the underlying mechanism is not well-understood. Small extracellular vesicles (sEVs) are emerging mediators of intercellular communication. Here, we investigated the role of KC-derived sEVs in the Th1 and Th17 response in psoriasis. We isolated and characterized sEVs from KCs under normal (untreated) and psoriatic (cytokine-treated) conditions. sEVs under both conditions exhibited a cup-shaped morphology and expressed markers CD63 and CD81. sEVs from cytokine-treated KCs can be taken up by CD4+T cells, leading to the induction of Th1 and Th17 polarization. Small RNA sequencing revealed that miR-381-3p was significantly increased in sEVs from cytokine-treated KCs and in CD4+T cells from patients with psoriasis. Moreover, sEVs-containing miR-381-3p was responsible for sEVs-induced Th1 and Th17 polarization. We further found that the miR-381-3p targeted to the 3′ untranslated region of E3 ubiquitin-ligase UBR5 and stabilized RORγt protein expression. It also targeted to the 3′ untranslated region of FOXO1, associated with activated T-bet and RORγt transcription. Taken together, we propose that psoriatic KCs transfer miR-381-3p to CD4+T cells through sEVs, inducing Th1 and Th17 polarization and promoting psoriasis development. Our findings motivate future studies of KC-derived sEVs or their specific cargoes as therapeutic candidates for psoriasis." @default.
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• W3044089550 date "2021-03-01" @default.
• W3044089550 modified "2023-10-18" @default.
• W3044089550 title "Small Extracellular Vesicles Containing miR-381-3p from Keratinocytes Promote T Helper Type 1 and T Helper Type 17 Polarization in Psoriasis" @default.
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• W3044089550 doi "https://doi.org/10.1016/j.jid.2020.07.009" @default.
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• W3044089550 hasPublicationYear "2021" @default.
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