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Galectin-1 induced activation of the apoptotic death-receptor pathway in human Jurkat T lymphocytes

Bettina Brandt1, Tom Büchse, Ehab Fathi Abou-Eladab

  • 1Medical Faculty, Institute of Medical Biochemistry and Molecular Biology, University of Rostock, Schillingallee 70, 18057 Rostock, Germany.

Histochemistry and Cell Biology
|February 22, 2008
PubMed

Insights

Galectin-1 (gal-1) triggers apoptosis in Jurkat T-cells by binding to Fas receptors and activating caspases. This interaction highlights gal-1

Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Galectin-1 (gal-1) is a beta-galactoside binding protein involved in immune regulation, cell growth, and apoptosis.
  • The Fas (Apo-1/CD95) receptor pathway is crucial for initiating programmed cell death (apoptosis).

Purpose of the Study:

  • To investigate if galectin-1 influences the Fas-associated apoptosis cascade in T-cell lines.
  • To determine the mechanism by which gal-1 interacts with the Fas pathway.

Main Methods:

  • Utilized Jurkat and MOLT-4 T-cell lines.
  • Induced apoptosis using gal-1 and anti-Fas antibodies.
  • Assessed DNA fragmentation and caspase activation.
  • Employed immunofluorescence, protein binding assays, immunoblotting, and LC-MS/MS to identify gal-1 targets.

Main Results:

  • Galectin-1 induced DNA fragmentation in Jurkat cells, but not in MOLT-4 cells.
  • This effect was blocked by caspase-8 inhibitors and neutralizing anti-Fas antibodies.
  • Fas was identified as a direct binding target for gal-1.
  • Gal-1 promoted the activation and processing of procaspase-8 and procaspase-3.

Conclusions:

  • Galectin-1 directly targets Fas receptors on T-cells, initiating the apoptotic pathway.
  • Gal-1 binding to Fas leads to caspase-8 activation and subsequent downstream apoptosis.
  • These findings reveal a novel mechanism of gal-1-mediated apoptosis through the Fas death-receptor pathway.

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