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Updated: Jun 8, 2026

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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
Regulatory T cell enrichment by IFN-γ conditioning
Gang Feng1, Kathryn J Wood, Andrew Bushell
1Transplantation Research Immunology Group, Nuffield Department of Surgery, John Radcliffe Hospital, University of Oxford, Oxford, UK.
Methods in Molecular Biology (Clifton, N.J.)
|October 14, 2010
Summary
Interferon-gamma (IFN-γ) can paradoxically promote the generation of regulatory T cells (Treg), which are crucial for preventing transplant rejection. This finding suggests a novel feedback loop in immune regulation.
Area of Science:
- Immunology
- Transplantation immunology
- Cellular therapy
Background:
- Interferon-gamma (IFN-γ) was initially known for its pro-inflammatory role in T helper type 1 responses.
- Regulatory T cells (Treg) are vital for managing autoimmunity, graft-versus-host disease (GVHD), and transplantation.
- Ex vivo generation of Treg is essential for their therapeutic application in preventing allograft rejection.
Purpose of the Study:
- To investigate the potential of using IFN-γ in the ex vivo generation and expansion of alloantigen-reactive Treg.
- To explore the paradoxical role of IFN-γ in the context of allograft survival and immune regulation.
Main Methods:
- Experiments were conducted to generate and expand regulatory T cells ex vivo.
- The study focused on using IFN-γ as a key cytokine in the Treg generation protocol.
Main Results:
- Alloantigen-reactive regulatory T cells (Treg) were successfully generated and expanded ex vivo using IFN-γ.
- This finding contrasts with the traditional understanding of IFN-γ as a cytokine promoting allograft rejection.
Conclusions:
- IFN-γ exhibits a dual role, paradoxically supporting the generation of immune-suppressive Treg.
- This suggests a potential physiological negative feedback mechanism involving IFN-γ in immune responses.
- The findings open new avenues for Treg-based cellular therapies in transplantation.

