ArticleCellular signalling2021
Extracellular vesicles produced by primary human keratinocytes in response to TLR agonists induce stimulus-specific responses in antigen-presenting cells.
Article in Cellular signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Exosomes in nanomedicine: a promising cell-free therapeutic intervention in burn wounds.Stem cell research & therapy · 2024Review
- Autophagy-Dependent Secretion: Crosstalk between Autophagy and Exosome Biogenesis.Current issues in molecular biology · 2024Review
- Skin cell-derived extracellular vesicles: a promising therapeutic strategy for cutaneous injury.Burns & trauma · 2022Review
- Downregulation of miRNA miR-1305 and upregulation of miRNA miR-6785-5p may be associated with psoriasis.Frontiers in genetics · 2022Article
- Oropharyngeal tumor cells induce COX-2 expression in peripheral blood monocytes by secretion of IL-1α.Frontiers in immunology · 2022Article
- Potential Pathogenetic Role of Antimicrobial Peptides Carried by Extracellular Vesicles in an in vitro Psoriatic Model.Journal of inflammation research · 2022Article
- Extracellular vesicles: Function, resilience, biomarker, bioengineering, and clinical implications.Tzu chi medical journalReview
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
Cells can communicate through the extracellular vesicles (EVs) they secrete. Pathogen associated molecular patterns (PAMPs), alter the biophysical and communicative properties of EVs released from cells, but the functional consequences of these changes are unknown. Characterization of keratinocyte-derived EVs after poly(I:C) treatment (poly(I:C)-EVs) showed slight differences in levels of EV markers TSG101 and Alix, a loss of CD63 and were positive for autophagosome marker LC3b-II and the cytokine IL36γ compared to EVs from unstimulated keratinocytes (control-EVs). Flagellin treatment (flagellin-EVs) led to an EV marker profile like control-EVs but lacked LC3b-II. Flagellin-EVs also lacked IL-36γ despite nearly identical intracellular levels. While poly(I:C) treatment led to the clear emergence of a > 200 nm diameter EV sub-population, these were not found in flagellin-EVs. EV associated IL-36γ colocalized with LC3b-II in density gradient analysis, equilibrating to 1.10 g/mL, indicating a common EV species. Poly(I:C), but not flagellin, induced intracellular vesicles positive for IL-36γ, LC3b-II, Alix and TSG101, consistent with fusion of autophagosomes and multivesicular bodies. Simultaneous rapamycin and flagellin treatment induced similar intracellular vesicles but was insufficient for the release of IL-36γ
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.