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Adenoviral Transduction of Naive CD4 T Cells to Study Treg Differentiation
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Adenoviral Transduction of Naive CD4 T Cells to Study Treg Differentiation

Published on: August 13, 2013

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The transcription factor musculin promotes the unidirectional development of peripheral Treg cells by suppressing the

Chuan Wu1, Zuojia Chen1, Valerie Dardalhon1

  • 1Evergrande Center for Immunologic Diseases, Harvard Medical School and Brigham and Women's Hospital, Boston, Massachusetts, USA.

Nature Immunology
|January 24, 2017
PubMed

Insights

Musculin (MSC) is a crucial transcription factor for developing regulatory T cells (Treg cells). It represses T helper 2 (TH2) cell programs, ensuring Treg cell function and preventing inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Master transcription factors (TFs) direct T cell subset development.
  • The role of additional transcriptional regulators in suppressing alternative T cell lineages remains unclear.

Purpose of the Study:

  • To identify transcriptional regulators involved in induced regulatory T cell (iTreg) development.
  • To elucidate the mechanism by which iTreg cells suppress other T cell lineages.

Main Methods:

  • Investigated the role of TF musculin (MSC) in TGF-β-induced iTreg cell differentiation.
  • Analyzed the impact of MSC on Foxp3 expression and T helper 2 (TH2) cell transcriptional programs.
  • Examined GATA-3 binding and intrachromosomal interactions in TH2 cytokine loci.

Main Results:

  • MSC is critical for iTreg cell development by repressing the TH2 program.
  • Loss of MSC reduced Foxp3 expression and promoted TH2 differentiation.
  • MSC inhibited GATA-3 binding to TH2 cytokine loci and diminished intrachromosomal interactions.
  • Msc-deficient iTreg cells failed to suppress TH2 responses, and Msc-deficient mice developed gut and lung inflammation.

Conclusions:

  • MSC enforces Foxp3 expression and promotes unidirectional iTreg cell induction.
  • MSC acts by repressing the TH2 developmental program, ensuring Treg cell stability and function.

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