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mTORC2 regulates multiple aspects of NKT-cell development and function.

Tammarah Sklarz1, Peng Guan2, Mercy Gohil1

  • 1Abramson Family Cancer Research Center, University of Pennsylvania, Philadelphia, PA, USA.

European Journal of Immunology
|January 13, 2017
PubMed
Summary
This summary is machine-generated.

The mechanistic target of rapamycin complex 2 (mTORC2) component Rictor is crucial for invariant natural killer T (iNKT) cell development and function. Rictor regulates iNKT cell survival, proliferation, and NKT-17 subset differentiation.

Keywords:
cytotoxicitydevelopmentdifferentiationnatural killer T cellsignal transductionthymus

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Area of Science:

  • Immunology
  • Cellular Biology
  • Molecular Biology

Background:

  • Invariant natural killer T (iNKT) cells are critical immune regulators bridging innate and adaptive immunity.
  • iNKT cell subsets (NKT-1, NKT-2, NKT-17) are defined by cytokine secretion profiles (IFN-γ, IL-4, IL-17A).
  • The role of Rictor, a component of mTORC2, in iNKT cell subset development is unclear due to conflicting reports.

Purpose of the Study:

  • To elucidate the role of Rictor in iNKT cell development and function.
  • To resolve conflicting data regarding Rictor's involvement in iNKT cell subset specification.
  • To investigate the impact of Rictor deficiency on iNKT cell numbers, survival, proliferation, and effector functions.

Main Methods:

  • Utilized Rictor conditional knockout mice (Rictorfl/fl CD4cre+).
  • Analyzed iNKT cell populations, cytokine production (IFN-γ, IL-4, IL-17A), and cytolytic activity.
  • Assessed iNKT cell survival and proliferation rates.

Main Results:

  • Rictor is essential for NKT-17 cell development.
  • Rictor deficiency leads to significantly reduced overall iNKT cell numbers.
  • Rictor is critical for maintaining iNKT cell survival and proliferation.
  • Cytolytic function of iNKT cells is impaired in the absence of Rictor.
  • IL-4 and IFN-γ production by peripheral iNKT cells remains substantial despite Rictor deficiency.

Conclusions:

  • mTORC2 signaling, mediated by Rictor, plays a multifaceted role in iNKT cell biology.
  • Rictor is indispensable for NKT-17 cell lineage commitment and overall iNKT cell homeostasis.
  • Rictor regulates both the development and effector functions of iNKT cells, impacting survival and proliferation.