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Foxp3 drives context-dependent epigenetic programs that define regulatory T cell molecular identity and function.

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Regulatory T cells (Treg cells) gain Foxp3 expression and function in vivo. Foxp3 drives Treg cell identity by shaping epigenetic landscapes and requires specific signaling pathways.

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Area of Science:

  • Immunology
  • Epigenetics
  • Cell Biology

Background:

  • Regulatory T cells (Treg cells) are crucial for immune homeostasis.
  • Foxp3 is the master regulator of Treg cells, but its role in establishing Treg cell identity is not fully understood.

Purpose of the Study:

  • To investigate the role of Foxp3 in driving Treg cell-specific epigenetic features and functions.
  • To identify the molecular mechanisms underlying Foxp3-mediated Treg cell induction.

Main Methods:

  • Utilized Foxp3-transduced conventional T cells in a gain-of-function model in mice.
  • Performed transcriptomic and chromatin profiling (ATAC-seq, ChIP-seq).
  • Analyzed signaling pathways including AKT-mTOR, STAT5, and NF-κB.

Main Results:

  • Identified a novel subset of T cells acquiring endogenous Foxp3 expression and Treg cell-like functions in vivo.
  • Demonstrated that Foxp3 is required for Treg cell-specific transcriptomic and chromatin features.
  • Revealed that Foxp3 induction necessitates reduced AKT-mTOR signaling and engagement of STAT5 and NF-κB.
  • Uncovered stepwise Foxp3-driven epigenetic programs, including a core and effector-specific programs.

Conclusions:

  • Foxp3 actively shapes the epigenetic landscape to establish and maintain Treg cell identity and function.
  • Foxp3 integrates intrinsic and environmental signals to drive Treg cell-specific gene expression.
  • Findings have implications for developing Foxp3-based immunotherapies.