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Related Experiment Video

Updated: Feb 24, 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

A Rogue Foxp3 Mutant Undermines Treg Cell Function.

¹Nomis Foundation Laboratories for Immunobiology and Microbial Pathogenesis, The Salk Institute for Biological Studies, 10010 N. Torrey Pines Road, La Jolla, CA 92037, USA.

|August 17, 2017

Summary

This summary is machine-generated.

A FOXP3 mutant in autoimmune IPEX disease broadens DNA binding, repressing Batf. This identifies Batf as crucial for regulatory T cell function and suggests FOXP3 DNA-binding changes may increase autoimmune disease susceptibility.

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Last Updated: Feb 24, 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

Adenoviral Transduction of Naive CD4 T Cells to Study Treg Differentiation

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Published on: August 13, 2013

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets

Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets

Published on: April 16, 2015

Area of Science:

Immunology
Genetics
Molecular Biology

Background:

Immune dysregulation, polyendocrinopathy, enteropathy, X-linked (IPEX) syndrome is a rare autoimmune disease.
The transcription factor FOXP3 is essential for the development and function of regulatory T cells (Tregs).

Purpose of the Study:

To investigate the functional consequences of a FOXP3 mutation found in IPEX patients.
To identify downstream targets of FOXP3 and their role in Treg function and autoimmune disease pathogenesis.

Main Methods:

Analysis of DNA-binding specificity of wild-type and mutant FOXP3.
Quantitative PCR and Western blotting to assess gene expression changes.
In vitro assays to evaluate the impact on Treg function.

Main Results:

A FOXP3 mutant exhibited broadened DNA-recognition specificity compared to wild-type FOXP3.
This mutant directly repressed the expression of the gene encoding the transcription factor Batf.
Batf was identified as a critical factor for tissue-resident Treg function.

Conclusions:

FOXP3 DNA-binding specificity is critical for maintaining Treg function and preventing autoimmunity.
Altered FOXP3 DNA-binding specificity, as seen in IPEX patients, can lead to immune dysregulation.
Polymorphisms affecting FOXP3 DNA-binding may represent a risk factor for developing autoimmune diseases.