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

Luke D Halder¹, Emeraldo A H Jo¹, Mohammad Z Hasan¹

¹Department of Infection Biology, Leibniz Institute for Natural Product Research and Infection Biology, 07745, Jena, Germany.

Nature Communications

|May 13, 2020

Summary

This summary is machine-generated.

Monocytes release TGF-β1-transporting vesicles upon encountering Candida albicans via complement receptor 3 (CR3). These vesicles suppress inflammation by inhibiting pro-inflammatory cytokine production, revealing a novel immune regulatory pathway.

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Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro

Simultaneous Study of the Recruitment of Monocyte Subpopulations Under Flow In Vitro

Published on: November 26, 2018

Area of Science:

Immunology
Cellular Biology
Microbiology

Background:

Extracellular vesicles mediate intercellular communication.
Monocytes play a key role in the immune response to pathogens like Candida albicans.

Purpose of the Study:

To investigate the role of monocytes in releasing TGF-β1-transporting vesicles in response to Candida albicans.
To elucidate the mechanism of vesicle release and their anti-inflammatory effects.

Main Methods:

Utilized CRISPR-CAS9 genome editing to generate CR3-deficient monocytes.
Isolated monocytes from CR3-deficient mice.
Assessed vesicle release and anti-inflammatory effects in human M1-macrophages and whole blood.
Investigated downstream signaling pathways including SMAD7.

Main Results:

Human and mouse monocytes release TGF-β1-transporting vesicles upon stimulation with Candida albicans.
Soluble β-glucan from C. albicans binds to complement receptor 3 (CR3) on monocytes, inducing vesicle release.
CR3-deficiency abrogates vesicle release.
These vesicles reduce pro-inflammatory responses and inhibit IL1B transcription.
Apoptotic bodies also induce similar TGF-β1-transporting vesicle production.

Conclusions:

Monocytes release TGF-β1-transporting vesicles in response to Candida albicans via a CR3-dependent mechanism.
These vesicles exert anti-inflammatory effects by modulating cytokine production and signaling pathways.
This pathway may represent an early immune suppression mechanism during fungal infections.