Level D· Scientific groundwork from lab and animal studiesAnimal StudyEurope PMCOpen access

WTAP/YTHDF1-mediated m<sup>6</sup>A modification amplifies IFN-γ-induced immunosuppressive properties of human MSCs

Chen Q., Ao L., Zhao Q., Tang L., Xiong Y., Yuan Y.

Animal Study, published in J Adv Res (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
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This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Animal Study
Journal
J Adv Res (2025)
Reported sample size
—
Source database
Europe PMC
PMID
38944238
PMCID
PMC12126738
DOI
10.1016/j.jare.2024.06.019
Citations
16

Abstract (original English)

Introduction The immunosuppressive capacity of mesenchymal stem cells (MSCs) is dependent on the "license" of several pro-inflammatory factors to express immunosuppressive molecular profiles, which determines the therapeutic efficacy of MSCs in immune-mediated inflammatory diseases. Of those, interferon-γ (IFN-γ) is a key inducer for the expression of immunosuppressive molecular profiles; however, the mechanism underlying this effect is unknown. Objectives To elucidate the regulation mechanism and biological functions of N 6 -methyladenosine (m 6 A) modification in the immunosuppressive functions by the IFN-γ-licensing MSCs. Methods Epitranscriptomic microarray analysis and MeRIP-qPCR assay were performed to identify the regulatory effect of WTAP in the IFN-γ-licensing MSCs. RIP-qPCR, western blot, qRT-PCR and RNA stability assays were used to determine the regulation of WTAP/m 6 A/YTHDF1 signaling axis in the expression of immunosuppressive molecules. Further, functional capacity of T cells was tested using flow cytometry, and both DSS-induced colitis mice and CIA mice were constructed to clarify the effect of WTAP and YTHDF1 in MSC-mediated immunosuppression. Results We identified that IFN-γ increased the m 6 A methylation levels of immunosuppressive molecules, while WTAP deficiency abolished the IFN-γ-induced promotion of m 6 A modification. IFN-γ activated ERK signaling, wh

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
T-LymphocytesMesenchymal Stem CellsAnimalsMice, Inbred C57BLHumansMiceColitisRNA-Binding ProteinsAdenosineSignal Transduction

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