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Related Experiment Video

Updated: Feb 4, 2026

In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol

In Vitro Differentiation of Human CD4⁺FOXP3⁺ Induced Regulatory T Cells (iTregs) from Naïve CD4⁺ T Cells Using a TGF-β-containing Protocol

Published on: December 30, 2016

Stabilization of Human CD8⁺ Treg in Inflammatory Environments Through FOXP3 Expression.

Séverine Bézie¹, Jenny Greig¹, Sonia Salle¹

¹Nantes Université, CHU Nantes, INSERM, Center for Research in Transplantation and Translational Immunology, UMR 1064, ITUN, Nantes, France.

European Journal of Immunology

|February 3, 2026

Summary

Regulatory T cells (Tregs) are promising for immune-mediated diseases, but stability is key. This study reveals how inflammation affects CD8+ Tregs and identifies FOXP3 and other molecules to enhance their stability for cell therapy.

Keywords:

CD8+ Tregs FOXP3 gene regulation inflammation stability

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Last Updated: Feb 4, 2026

In Vitro Differentiation of Human CD4+FOXP3+ Induced Regulatory T Cells (iTregs) from Naïve CD4+ T Cells Using a TGF-β-containing Protocol

In Vitro Differentiation of Human CD4⁺FOXP3⁺ Induced Regulatory T Cells (iTregs) from Naïve CD4⁺ T Cells Using a TGF-β-containing Protocol

Published on: December 30, 2016

Three-dimensional Inflammatory Human Tissue Equivalents of Gingiva

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Published on: April 3, 2018

Use of Single Chain MHC Technology to Investigate Co-agonism in Human CD8+ T Cell Activation

Use of Single Chain MHC Technology to Investigate Co-agonism in Human CD8+ T Cell Activation

Published on: February 28, 2019

Area of Science:

Immunology
Cell Biology
Therapeutics

Background:

Regulatory T cells (Tregs) show therapeutic potential for immune-mediated diseases.
Stability and persistence of transferred Tregs in inflammatory environments are critical challenges.
CD8+ Tregs possess plasticity due to cytokine receptor expression, raising questions about their stability.

Purpose of the Study:

Investigate the susceptibility of CD8+ Tregs to pro-inflammatory signals.
Determine the role of FOXP3 in maintaining CD8+ Treg stability.
Identify molecular targets to enhance Treg stability for cell therapy.

Main Methods:

Short-term and long-term cell cultures with various cytokines (IL-6, TNFα, IFNγ, TGFβ, IL-1β, IL-21, IL-23).
Transcriptomic analysis to assess changes in gene expression, including FOXP3.
Lentiviral transduction to enforce FOXP3 expression or introduce mTOR regulators (SESN2, FLCN) and SAGA complex component (TAF5L).
Assessment of Treg suppressive activity in vitro and phenotypic stability under inflammatory conditions.

Main Results:

Exposure to TGFβ combined with IL-6/IL-1β or IL-21/IL-23 induced significant transcriptomic changes and FOXP3 downregulation in CD8+ Tregs.
Enforced FOXP3 expression stabilized Treg phenotype and enhanced suppressive activity in vitro.
FOXP3 knockout CD8+ Tregs maintained suppressive function for up to 2 weeks.
Transduction of SESN2, FLCN, or TAF5L boosted FOXP3 expression, with SESN2 and TAF5L alone enhancing suppressive function.

Conclusions:

Pro-inflammatory cytokines, particularly TGFβ in combination with others, can destabilize CD8+ Tregs by downregulating FOXP3.
FOXP3 plays a crucial role in maintaining CD8+ Treg stability and function under inflammatory conditions.
Targeting FOXP3, SESN2, FLCN, or TAF5L presents a promising strategy for developing more stable and effective Treg-based cell therapies.