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.
journal_name
Nat Communjournal_title
Nature communicationsauthors
Halder LD,Jo EAH,Hasan MZ,Ferreira-Gomes M,Krüger T,Westermann M,Palme DI,Rambach G,Beyersdorf N,Speth C,Jacobsen ID,Kniemeyer O,Jungnickel B,Zipfel PF,Skerka Cdoi
10.1038/s41467-020-16241-5subject
Has Abstractpub_date
2020-05-11 00:00:00pages
2331issue
1issn
2041-1723pii
10.1038/s41467-020-16241-5journal_volume
11pub_type
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