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The kinases aurora B and mTOR regulate the G1-S cell cycle progression of T lymphocytes

Jianxun Song1, Shahram Salek-Ardakani, Takanori So

  • 1Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, La Jolla, California 92037, USA.

Nature Immunology
|November 28, 2006
PubMed

Insights

CD28-deficient T cells require aurora B kinase for cell cycle progression. This kinase, complexed with survivin and mammalian target of rapamycin (mTOR), regulates the G1-S checkpoint, restoring T cell proliferation and promoting inflammation.

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • T cell activation and proliferation are critical for adaptive immunity.
  • The CD28 co-stimulatory molecule plays a vital role in T cell responses.
  • Deficiency in CD28 leads to cell cycle arrest at the G1-S transition.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying cell cycle arrest in CD28-deficient T cells.
  • To identify key regulators of the G1-S checkpoint in T cells.
  • To explore the role of aurora B kinase in T cell proliferation and inflammation.

Main Methods:

  • Analysis of cell cycle progression in CD28-deficient T cells.
  • Investigation of the complex formation between aurora B, survivin, and mammalian target of rapamycin (mTOR).
  • Assessment of aurora B kinase activity and its downstream effects on cell cycle proteins.
  • Evaluation of T cell proliferation and in vivo inflammatory responses.

Main Results:

  • Aurora B kinase, in complex with survivin and mTOR, controls the G1-S transition in T cells.
  • Expression of aurora B in CD28-deficient T cells restored cell cycle progression by enhancing mTOR substrate phosphorylation, cyclin A expression, retinoblastoma protein hyperphosphorylation, and cyclin-dependent kinase activation.
  • Interleukin 2 enhanced aurora B activity, while its inhibition prevented interleukin 2-induced proliferation.
  • Restoration of aurora B expression rescued CD28-deficient T cell proliferation and promoted in vivo inflammation.

Conclusions:

  • Aurora B kinase, along with survivin and mTOR, acts as a crucial regulator of the G1-S checkpoint in T cells.
  • Targeting aurora B kinase may offer therapeutic strategies for modulating T cell responses and inflammation.

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