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Updated: Jun 19, 2026

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Mouse Naïve CD4+ T Cell Isolation and In vitro Differentiation into T Cell Subsets
Published on: April 16, 2015
CD4+ regulatory T cells control TH17 responses in a Stat3-dependent manner
Ashutosh Chaudhry1, Dipayan Rudra, Piper Treuting
1Howard Hughes Medical Institute and Immunology Program, Memorial Sloan-Kettering Cancer Center, New York, NY 10065, USA.
Summary
Regulatory T cells (Tregs) suppress pathogenic T helper 17 (Th17) immune responses by regulating STAT signaling. Loss of Treg-specific Stat3 impairs this suppression, leading to fatal inflammation.
Area of Science:
- Immunology
- Molecular Biology
- Genetics
Background:
- Distinct immune responses are mediated by STAT transcription factors.
- CD4+ regulatory T cells (Tregs) prevent autoimmunity by suppressing T helper 1 (Th1) and T helper 2 (Th2) responses.
- The role of Tregs in restraining pathogenic T helper 17 (Th17) responses remains less understood.
Purpose of the Study:
- To investigate the role of Tregs in suppressing pathogenic Th17 responses.
- To determine the involvement of STAT3 in Treg-mediated suppression of Th17 cells.
Main Methods:
- Treg-specific ablation of Stat3 in mice.
- Analysis of immune cell populations and cytokine profiles.
- Assessment of disease development and severity.
Main Results:
- Treg-specific ablation of Stat3 led to uncontrolled Th17 responses.
- This resulted in the development of fatal intestinal inflammation in mice.
- Tregs were shown to restrain pathogenic Th17 responses via Stat3-dependent mechanisms.
Conclusions:
- Tregs adapt their suppressive function based on the specific immune response, utilizing STAT proteins.
- Stat3 is critical for Treg-mediated suppression of Th17-driven inflammation.
- Targeting Treg-STAT interactions may offer therapeutic strategies for autoimmune diseases.
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