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Related Experiment Videos

Caspase activation is required for T cell proliferation.

N J Kennedy1, T Kataoka, J Tschopp

  • 1Immunobiology Program, Department of Medicine, The University of Vermont College of Medicine, Burlington, Vermont 05405, USA.

The Journal of Experimental Medicine
|December 22, 1999
PubMed
Summary

Fas death receptors surprisingly promote T cell growth and interleukin 2 production via caspase activation. This study reveals a dual role for death receptors in T cell proliferation and survival.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Fas (CD95) receptor triggering by Fas ligand (FasL) typically induces apoptosis via caspase cascade activation.
  • Recent findings showed FADD-deficient T cells resistant to FasL-induced apoptosis but with impaired proliferation, suggesting dual roles for Fas.
  • The precise role of caspases in T cell activation and proliferation remained unclear.

Purpose of the Study:

  • To investigate the role of caspases in T cell proliferation and interleukin 2 production.
  • To explore the involvement of death receptors, specifically Fas, in T cell activation.
  • To elucidate the dual functions of death receptors in both T cell death and growth.

Main Methods:

  • Utilized caspase inhibitors to block CD3-induced T cell proliferation and IL-2 production.

Related Experiment Videos

  • Analyzed caspase-8 and caspase-3 processing following CD3 stimulation.
  • Employed Fas-Fc and soluble FasL to assess their impact on T cell proliferation.

    • Main Results:

    • Caspase activity inhibition blocked CD3-induced T cell proliferation and IL-2 production.
    • CD3 stimulation led to rapid caspase-8 cleavage, but not caspase-3 processing.
    • Fas-Fc inhibited T cell proliferation, while soluble FasL enhanced it.

    Conclusions:

    • Caspases play a crucial role in promoting T cell activation and proliferation.
    • Death receptors, like Fas, exhibit a dual role in T cell biology, mediating both death and growth.
    • TCR-mediated upregulation of FasL contributes to T cell proliferation in a caspase-dependent manner.