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Updated: Jun 28, 2026

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
Foxp1 controls Fezf2-dependent gene expression, mimetic mTEC diversity, and thymic central tolerance
Jun Hyung Sin1,2, Christopher J Bowman3, Juliana Sucharov1
1Biomedical Sciences Graduate Program, University of California, San Francisco, United States.
Forkhead Box P1 (Foxp1) regulates thymic epithelial cell populations. Its deletion alters medullary thymic epithelial cell diversity, impacting immune tolerance and potentially causing autoimmunity.
Area of Science:
- Immunology
- Developmental Biology
- Transcription Factor Biology
Background:
- Forkhead Box P1 (Foxp1) is a crucial transcription factor for tissue development.
- Foxp1 is known to regulate T and B cell adaptive immunity.
- Its role in medullary thymic epithelial cells (mTECs) was previously unreported.
Purpose of the Study:
- To investigate the function of Foxp1 in mTECs.
- To determine the impact of Foxp1 deletion on mTEC populations and thymic function.
Main Methods:
- Conditional deletion of Foxp1 in thymic epithelial cells (TECs).
- Analysis of mTEC populations using flow cytometry and single-cell RNA sequencing (scRNA-seq).
- Assessment of thymic size, lymphocyte populations, and B cell class switching.
Main Results:
- Foxp1 deletion in TECs led to significant mTEC population changes.
- Expansion of neuroendocrine and Ccl21a-expressing mTECs, with a loss of Aire, tuft, and microfold mTECs.
- Alterations in thymic size, innate lymphocyte populations, and impaired B cell class switching were observed.
- Decreased Fezf2 expression in Foxp1-deleted mTECs attenuated tissue-specific antigen expression, leading to autoimmunity in aged mice.
Conclusions:
- Foxp1 is a key regulator of mTEC diversity and function.
- Foxp1 influences Fezf2-dependent gene expression, impacting self-antigen presentation.
- Dysregulation of Foxp1 in mTECs contributes to altered thymic immunity and autoimmunity.
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