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Mammalian target of rapamycin complex 2 modulates αβTCR processing and surface expression during thymocyte
Po-Chien Chou1, Won Jun Oh1, Chang-Chih Wu1
1Department of Biochemistry and Molecular Biology, Rutgers-Robert Wood Johnson Medical School, Piscataway, NJ 08854;
Journal of Immunology (Baltimore, Md. : 1950)
|July 2, 2014
Summary
Deletion of mTORC2 component rictor impairs T cell development by reducing surface receptor expression. This leads to aberrant maturation and developmental blocks in thymocytes, impacting immune response.
Area of Science:
- Immunology
- Cell Biology
- Molecular Biology
Background:
- T cell receptor (TCR) diversity is crucial for immune response.
- Mechanisms controlling TCR surface expression are less understood than TCR diversity generation.
Purpose of the Study:
- To investigate the role of mTORC2 in T cell development and receptor surface expression.
- To understand how rictor deletion affects T cell maturation and signaling.
Main Methods:
- Studied T cell development in mice lacking the rictor component of mTORC2.
- Analyzed surface expression of TCR and other key receptors (CD4, CD8, CD69, Notch, CD147) on thymocytes.
- Assessed T cell proliferation and developmental progression.
Main Results:
- Rictor deletion caused aberrant T cell maturation and increased TCR proteasomal degradation.
- Surface levels of TCR, CD4, CD8, CD69, Notch, and CD147 were significantly reduced.
- Defective receptor expression led to impaired signaling, proliferation, and developmental blocks at multiple thymocyte stages.
Conclusions:
- mTORC2, via rictor, is essential for proper T cell development.
- mTORC2 regulates the co/posttranslational processing and surface expression of membrane receptors.
- Rictor-mediated mTORC2 signaling impacts T cell differentiation by controlling receptor quantity and quality.
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