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Updated: Mar 20, 2026
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3D Organotypic Co-culture Model Supporting Medullary Thymic Epithelial Cell Proliferation, Differentiation and Promiscuous Gene Expression
Published on: July 30, 2015
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mTORC2 in Thymic Epithelial Cells Controls Thymopoiesis and T Cell Development
Hong-Xia Wang1, Joyce S Cheng2, Shuai Chu1
1Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong 510515, China; Division of Allergy and Immunology, Department of Pediatrics, Duke University Medical Center, Durham, NC 27710;
Journal of Immunology (Baltimore, Md. : 1950)
|May 29, 2016
Summary
Mechanistic target of rapamycin complex 2 (mTORC2) signaling in thymic epithelial cells (TECs) is crucial for T cell development. Ablating Rictor in TECs impairs thymic structure and reduces T cell generation.
Area of Science:
- Immunology
- Cell Biology
- Developmental Biology
Background:
- Thymic epithelial cells (TECs) are essential for T cell development.
- The precise mechanisms regulating TEC function and development remain incompletely understood.
- Mammalian or mechanistic target of rapamycin complex 2 (mTORC2) is involved in regulating cell survival, metabolism, and nutrient uptake.
Purpose of the Study:
- To investigate the role of mTORC2 signaling in TECs during thymopoiesis.
- To determine the impact of Rictor ablation in TECs on T cell generation.
Main Methods:
- Generated mice with TEC-specific ablation of Rictor, a key component of mTORC2.
- Analyzed thymic structure, TEC populations, and T cell lineage generation in these mice.
Main Results:
- TEC-specific Rictor deficiency led to thymic atrophy and reduced medullary TEC numbers.
- The generation of diverse T cell lineages, including TCRαβ, regulatory T cells, invariant NKT, and TCRγδ T cells, was significantly decreased.
- These findings highlight the importance of mTORC2 signaling within TECs.
Conclusions:
- mTORC2 signaling in TECs is critical for maintaining thymic architecture.
- Normal thymopoiesis and efficient generation of multiple T cell lineages depend on mTORC2 activity in TECs.
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