Matches in SemOpenAlex for { <https://semopenalex.org/work/W3022935852> ?p ?o ?g. }
- W3022935852 abstract "Abstract Extracellular vesicles have an important function in cellular communication. Here, we show that human and mouse monocytes release TGF-β1-transporting vesicles in response to the pathogenic fungus Candida albicans . Soluble β-glucan from C. albicans binds to complement receptor 3 (CR3, also known as CD11b/CD18) on monocytes and induces the release of TGF-β1-transporting vesicles. CR3-dependence is demonstrated using CR3-deficient (CD11b knockout) monocytes generated by CRISPR-CAS9 genome editing and isolated from CR3-deficient (CD11b knockout) mice. These vesicles reduce the pro-inflammatory response in human M1-macrophages as well as in whole blood. Binding of the vesicle-transported TGF-β1 to the TGF-β receptor inhibits IL1B transcription via the SMAD7 pathway in whole blood and induces TGFB1 transcription in endothelial cells, which is resolved upon TGF-β1 inhibition. Notably, human complement-opsonized apoptotic bodies induce production of similar TGF-β1-transporting vesicles in monocytes, suggesting that the early immune response might be suppressed through this CR3-dependent anti-inflammatory vesicle pathway." @default.
- W3022935852 created "2020-05-13" @default.
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- W3022935852 date "2020-05-11" @default.
- W3022935852 modified "2023-10-15" @default.
- W3022935852 title "Immune modulation by complement receptor 3-dependent human monocyte TGF-β1-transporting vesicles" @default.
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- W3022935852 doi "https://doi.org/10.1038/s41467-020-16241-5" @default.
- W3022935852 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7214408" @default.
- W3022935852 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/32393780" @default.
- W3022935852 hasPublicationYear "2020" @default.
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