Immune modulation by complement receptor 3-dependent human monocyte TGF-β1-transporting vesicles

Luke D. Halder, Emeraldo A. H. Jo, Mohammad Z. Hasan, Marta Ferreira-Gomes, Thomas Krüger, Martin Westermann, Diana I. Palme, Günter Rambach, Niklas Beyersdorf, Cornelia Speth, Ilse D. Jacobsen, Olaf Kniemeyer, Berit Jungnickel, Peter F. Zipfel and Christine Skerka ()
Additional contact information
Luke D. Halder: Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology
Emeraldo A. H. Jo: Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology
Mohammad Z. Hasan: Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology
Marta Ferreira-Gomes: Department of Cell Biology, Institute of Biochemistry and Biophysics, Friedrich Schiller University
Thomas Krüger: Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology
Martin Westermann: Electron Microscopy Center, University Hospital Jena
Diana I. Palme: Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology
Günter Rambach: Division of Hygiene and Medical Microbiology, Medical University of Innsbruck
Niklas Beyersdorf: Institute for Virology and Immunobiology, University of Würzburg
Cornelia Speth: Division of Hygiene and Medical Microbiology, Medical University of Innsbruck
Ilse D. Jacobsen: Research Group Microbial Immunology, Leibniz Institute for Natural Product Research and Infection Biology
Olaf Kniemeyer: Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology
Berit Jungnickel: Department of Cell Biology, Institute of Biochemistry and Biophysics, Friedrich Schiller University
Peter F. Zipfel: Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology
Christine Skerka: Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology

Nature Communications, 2020, vol. 11, issue 1, 1-19

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.

Date: 2020
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/s41467-020-16241-5 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-16241-5

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-020-16241-5

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().