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Runx3 instructs Aire+ mTEC development, TSA gene expression, and central tolerance.

Jun Hyung Sin1, Sloan H Phillips2, Audrey V Parent3

  • 1Biomedical Sciences Graduate Program, University of California San Francisco, San Francisco, CA, USA; Department of Pediatrics, University of California San Francisco, San Francisco, CA, USA.

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Runx3 is crucial for medullary thymic epithelial cell (mTEC) development and function. Loss of Runx3 impairs the development of Autoimmune Regulator-positive mTECs and tissue-specific antigen expression, leading to autoimmunity.

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Area of Science:

  • Immunology
  • Developmental Biology
  • Molecular Biology

Background:

  • Runx3 is a transcription factor involved in tissue development.
  • Medullary thymic epithelial cells (mTECs) are essential for immune tolerance.
  • Autoimmune Regulator (Aire) and tissue-specific antigens (TSAs) are critical for mTEC function.

Purpose of the Study:

  • To investigate the role of Runx3 in thymic epithelial lineage development.
  • To determine the necessity of Runx3 in mTEC development and function.
  • To understand the impact of Runx3 deficiency on thymic central tolerance.

Main Methods:

  • Conditional knockout mice with TEC-specific Runx3 deletion.
  • Flow cytometry analysis of thymic populations.
  • Single-cell RNA sequencing.
  • Gene expression analysis of TSA and Aire.

Main Results:

  • TEC-specific Runx3 deletion significantly reduced Aire-positive mTECs.
  • Runx3 deficiency led to a global loss of TSA gene expression.
  • Loss of Runx3 resulted in an expansion of immature CCL21+ mTECs and a loss of Aire-dependent mimetic cells, causing autoimmunity.
  • Single-cell analysis revealed Runx3 modulates core transcriptional programs in TECs.

Conclusions:

  • Runx3 plays a previously undescribed role in mTEC development.
  • Runx3 is required for Aire+ mTEC development and TSA expression.
  • Runx3 is essential for maintaining thymic central tolerance and preventing autoimmunity.