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Measuring Composition of CD95 Death-Inducing Signaling Complex and Processing of Procaspase-8 in this Complex
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Fas(CD95)/FasL interactions required for programmed cell death after T-cell activation

S T Ju1, D J Panka, H Cui

  • 1Arthritis Center, Boston University School of Medicine, Massachusetts 02118.

Nature
|February 2, 1995
PubMed

Insights

Receptor crosslinking activates T-cells, leading to cell death. This process involves Fas ligand and Fas, which trigger the cell-death program, revealing key molecular mechanisms in T-cell apoptosis.

Area of Science:

  • Immunology
  • Molecular Biology
  • Cell Biology

Background:

  • T-cell activation by receptor crosslinking results in apoptosis.
  • The specific gene products mediating this activation-induced cell death (AICD) were previously unidentified.
  • AICD necessitates new RNA and protein synthesis.

Purpose of the Study:

  • To identify the specific gene products responsible for T-cell death following receptor crosslinking.
  • To elucidate the molecular mechanism underlying activation-induced T-cell death.

Main Methods:

  • Utilized T-cell hybridomas for experimental models.
  • Investigated the role of Fas ligand and Fas upregulation upon receptor crosslinking.
  • Employed a soluble Fas-immunoglobulin fusion protein to block Fas-mediated signaling.

Main Results:

  • Receptor crosslinking was found to induce Fas ligand and upregulate Fas expression on T-cells.
  • The interaction between Fas ligand and Fas was shown to activate the cell-death pathway.
  • A soluble Fas-immunoglobulin fusion protein selectively inhibited cell death, but not initial activation.

Conclusions:

  • Fas ligand and Fas are the critical death-gene products mediating activation-induced T-cell death.
  • The engagement of Fas by Fas ligand represents the core molecular mechanism of AICD.
  • These findings clarify the pathway leading to T-cell apoptosis after stimulation.

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