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Related Experiment Video

Updated: Sep 9, 2025

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo

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Published on: July 20, 2019

IFN-γ-Induced CD317 Tethers Extracellular Vesicles to Mesenchymal Stromal Cells Interfering With Immune Modulation.

Anton Selich¹, Luisa Weisskoeppel¹, Ralf Hass²

¹Institute of Experimental Hematology, Hannover Medical School, Hannover, Germany.

Journal of Extracellular Vesicles

|August 29, 2025

Summary

Activating mesenchymal stromal cells (MSCs) with interferon-gamma (IFN-γ) for longer periods increases CD317 expression, which hinders MSC-extracellular vesicle (EV) immune modulation. Reducing CD317 enhances therapeutic efficacy.

Keywords:

CD317/tetherin extracellular vesicles immune modulation mesenchymal stromal cells

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Last Updated: Sep 9, 2025

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Published on: May 10, 2022

Area of Science:

Immunology
Cell Biology
Biotechnology

Background:

Mesenchymal stromal cells (MSCs) and their extracellular vesicles (EVs) show therapeutic potential but face challenges due to inconsistent parameters.
Pro-inflammatory activation of MSCs using interferon-gamma (IFN-γ) and tumor necrosis factor-alpha (TNF-α) is widely accepted to enhance immune modulation.
The impact of activation duration on MSC-EV immune modulation remains underexplored.

Purpose of the Study:

To investigate the effect of MSC activation duration on MSC-EV-mediated immune modulation of macrophages.
To elucidate the role of CD317 in MSC-EV accumulation and immune modulation.

Main Methods:

MSCs were activated with IFN-γ and TNF-α for varying durations.
Flow cytometry was used to analyze CD317 expression on MSCs.
EV accumulation on MSC surfaces was assessed after activation or CD317 manipulation (overexpression/knockdown).
MSC-EV-mediated immune modulation of macrophages was evaluated.

Main Results:

Extended MSC activation (24 hours) led to increased IFN-γ-induced CD317 expression on the MSC surface.
CD317 was found to mediate the accumulation of EVs on the MSC cell surface.
CD317 knockdown eliminated EV surface enrichment and significantly enhanced MSC-EV-mediated immune modulation of macrophages.

Conclusions:

CD317 acts as a modulator of MSC-EV accumulation on the cell surface.
Reducing CD317 expression enhances the immune modulatory capacity of MSC-EVs.
Targeting CD317 could be a strategy to improve the efficacy of MSC-based therapies in clinical settings.