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Related Experiment Video

Updated: Jan 11, 2026

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A Notch too far: Treg plasticity in multiple sclerosis.

Justine Fiefvet1, Lidia Yshii1

  • 1Department of Neurosciences, Leuven Brain Institute, KU Leuven, Leuven, Belgium.

Immunity
|November 12, 2025
PubMed
Summary

Regulatory T cells (Tregs) can promote or suppress autoimmune inflammation. Gut-microbiota-induced Notch3+ Tregs migrate to the central nervous system in multiple sclerosis and become inflammatory Th17-like cells.

Area of Science:

  • Immunology
  • Neuroinflammation
  • Microbiome research

Background:

  • Regulatory T cells (Tregs) play complex roles in autoimmune diseases, potentially exacerbating or ameliorating inflammation.
  • The gut microbiota influences immune cell function and migration, impacting central nervous system (CNS) autoimmunity.

Purpose of the Study:

  • To investigate the role and behavior of gut-microbiota-induced regulatory T cells in the context of multiple sclerosis (MS).
  • To determine the specific subset of regulatory T cells involved and their differentiation pathways within the CNS.

Main Methods:

  • Analysis of immune cell populations in preclinical models of CNS autoimmunity and human samples.
  • Tracking the migration and differentiation of specific regulatory T cell subsets.

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Main Results:

  • Gut-microbiota-induced regulatory T cells expressing Notch3 (Notch3+ Tregs) were identified.
  • These Notch3+ Tregs were found to migrate from the gut to the CNS in models of MS.
  • Within the CNS, these cells transitioned into pro-inflammatory Th17-like cells, contributing to neuroinflammation.

Conclusions:

  • Gut-microbiota-induced Notch3+ regulatory T cells are implicated in the pathogenesis of multiple sclerosis.
  • These cells exhibit plasticity, converting into inflammatory phenotypes within the CNS.
  • Targeting these specific regulatory T cell subsets may offer novel therapeutic strategies for MS.