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  3. Normal Treg Homeostasis And Suppressive Function Require Both Foxp1 And Foxp4.
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  3. Normal Treg Homeostasis And Suppressive Function Require Both Foxp1 And Foxp4.

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Normal Treg homeostasis and suppressive function require both FOXP1 and FOXP4.

Dachuan Dong1,2,3, Vishal J Sindhava4, Ananthakrishnan Ganesan3

  • 1Geriatric Research Education and Clinical Center, Veterans Administration Palo Alto Health Care System, Palo Alto, California, USA.

JCI Insight
|August 12, 2025

View abstract on PubMed

Summary
This summary is machine-generated.

FOXP1 and FOXP4 proteins are crucial for regulatory T cell (Treg) function. Their combined absence in Tregs leads to immune dysfunction, autoimmunity, and early death in mice.

Keywords:
Adaptive immunityAutoimmunityImmunologyTregs

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Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • FOXP3+ regulatory T cells (Tregs) are essential for maintaining immune tolerance.
  • FOXP1 is known to influence Treg function, but FOXP4's role is largely uncharacterized.
  • Understanding FOXP family interactions in Tregs is critical for immune regulation.

Purpose of the Study:

  • To investigate the functional interactions between FOXP1 and FOXP4 in mouse Treg cells.
  • To determine the consequences of combined FOXP1 and FOXP4 deficiency in Tregs.

Main Methods:

  • Generation of mouse models with specific genetic deletion of Foxp1, Foxp4, or both in Treg cells.
  • Analysis of Treg cell phenotype, suppressive function, and immune responses.
  • Investigation of FOXP1 and FOXP4 binding to the Il2ra promoter.

Main Results:

  • Combined deficiency of FOXP1 and FOXP4 in Tregs caused lymphoproliferation, inflammation, autoimmunity, and early lethality.
  • Absence of both proteins led to an activated Treg phenotype, impaired suppressive function, enhanced germinal center response, and increased proinflammatory cytokine production.
  • FOXP1 and FOXP4 were found to regulate CD25 expression by binding to Il2ra promoter regions.

Conclusions:

  • FOXP1 and FOXP4 play non-redundant but cooperative roles in Treg cell function.
  • FOXP4 has an insufficient role alone, highlighting the importance of FOXP1 in Treg-mediated immune tolerance.
  • Combined FOXP1/FOXP4 deficiency severely disrupts Treg function, leading to autoimmune disease.