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Retroviral CRISPR/Cas9-Mediated Gene Targeting for the Study of Th17 Differentiation in Vitro

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Mesenchymal stem cell-derived extracellular vesicles subvert Th17 cells by destabilizing RORγt through

Sunyoung Jung^1,2, Sunho Lee^1,2, Hyun Je Kim^2,3,4,5

¹Department of Microbiology and Immunology, Seoul National University College of Medicine, Seoul, 03080, Korea.

Experimental & Molecular Medicine

|March 25, 2023

Summary

Mesenchymal stem cell small extracellular vesicles (MSC-sEVs) convert T helper 17 cells into low-IL-17 producers by degrading RORγt. This mechanism ameliorates autoimmune disease in mice, highlighting MSC-sEVs as a potential therapy.

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Characterization of Immune Cell-derived Extracellular Vesicles and Studying Functional Impact on Cell Environment

Characterization of Immune Cell-derived Extracellular Vesicles and Studying Functional Impact on Cell Environment

Published on: June 2, 2020

Area of Science:

Immunology
Cell Biology
Extracellular Vesicles

Background:

Mesenchymal stem cell-derived small extracellular vesicles (MSC-sEVs) possess known immunosuppressive properties.
T helper 17 (Th17) cells play a critical role in various inflammatory diseases.

Purpose of the Study:

To elucidate the specific immunosuppressive mechanism of MSC-sEVs on Th17 cells.
To investigate the role of RAR-related orphan receptor γt (RORγt) in MSC-sEV-mediated immunosuppression.
To evaluate the therapeutic potential of MSC-sEVs in experimental autoimmune encephalomyelitis (EAE).

Main Methods:

Treatment of experimental autoimmune encephalomyelitis (EAE) mice with MSC-sEVs.
Analysis of Th17 cell populations and RORγt protein levels in vivo and in vitro.
Investigation of MSC-sEVs' effect on RORγt ubiquitination and acetylation.
Manipulation of EP300-interacting inhibitor of differentiation 3 (Eid3) expression in MSCs and Th17 cells.

Main Results:

MSC-sEVs convert Th17 cells into IL-17 low-producing (ex-Th17) cells by degrading RORγt protein.
MSC-sEV treatment ameliorated EAE clinical symptoms and reduced Th17 cell infiltration in lymphoid organs and the CNS.
MSC-sEVs destabilize RORγt via K63 deubiquitination and deacetylation, mediated by Eid3.
Eid3 knockdown in MSCs abrogated RORγt downregulation, while Eid3 overexpression decreased RORγt levels in Th17 cells.

Conclusions:

MSC-sEVs exert immunosuppression by targeting RORγt degradation in Th17 cells through Eid3.
This novel mechanism highlights MSC-sEVs as a promising therapeutic strategy for Th17-mediated inflammatory diseases.